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In addition to OS, low body mass index BMI and malnutrition protectioj suggested to correlate with protectoin severity of COPD King et al. Underweight COPD patients tend to experience more pulmonary damage, exercise intolerance, and increased mortality rates, Antioxidanr comparison to individuals with normal weights King et al.
Malnutrition can lead to respiratory muscle mass reduction, which lowers the strength and endurance of these muscles Ferreira et al. In addition, decreased intake or availability of dietary antioxidants such as vitamins C and E, carotenoids, and polyphenols, can weaken the antioxidant system and exacerbate disease progression Figure 1 and Table 1 Sies et al.
A dietary pattern that is rich in vegetables, fruits, fish, and whole grains has been associated with improved pulmonary function and a lower risk of COPD Varraso et al.
It is suggested that nutritional supplementation enhances respiratory muscle function in malnourished COPD patients, thereby improving their quality of life Ferreira et al. For example, Hornikx et al.
As the most well-known nutritional antioxidant, vitamin C is capable of reducing oxidative damages and inflammation in the pulmonary system by scavenging excess ROS and activating NF-κB pathway, respectively Tecklenburg et al.
Furthermore, melatonin, a powerful antioxidant and a regulator of the sleep-wake cycle, can also attenuate OS-related lung deterioration Figure 1 and Table 1 Gumral et al. These findings support the potential use of nutritional antioxidants as an adjuvant to COPD treatment.
Similarly, several observational studies suggest that nutritional antioxidants from diets or supplements can improve asthma control and lung function in asthmatic patients Moreno-Macias and Romieu, A systematic review has proposed that there is an inverse association between dietary intake of vitamins A and C and incidence of asthma Table 1 Allen et al.
Vitamin C functions in conjunction with vitamin E to stimulate the regeneration of membrane-bound α-tocopherol from its oxidized states Moreno-Macias and Romieu, In addition, dietary carotenoids have been shown to correlate with improved asthma outcomes and lung function Wood et al.
The linkage between OS and the development of respiratory diseases suggests a pivotal role of nutritional antioxidants Romieu, Vulnerable populations include those with deficiency in dietary antioxidants, increased exposure to environmental sources of oxidants, and poor access to nutritional antioxidants Moreno-Macias and Romieu, It is important to note that although antioxidants may help to mitigate the progression of respiratory diseases, antioxidant supplements can act as pro-oxidants or OS inducers if consumed at levels that significantly surpass the recommended dietary intake Pham-Huy et al.
The potential benefits and risks of nutritional antioxidant supplementation trials in respiratory diseases should be considered on a case-by-case basis. Furthermore, it remains unknown whether OS is a consequence or the causative factor for some pulmonary diseases.
Therefore, antioxidant treatment may not be an effective approach to modify disease progression although it may be able to alleviate OS-related symptoms Margaritelis, Cardiovascular diseases CVD are the leading cause of mortality in the United States, resulting in nearly one million deaths each year Madamanchi et al.
The majority of CVD is correlated with atherosclerosis development, in which OS play a causal role Madamanchi et al.
Excessive ROS can be generated in vascular cells from NAD P H oxidase Noxnitric oxide synthases NOS uncoupling, and mitochondria, which cause oxidative modifications of low density lipoprotein LDL Azumi et al.
The oxidized LDL ox-LDL transported through the arterial lumens induces apoptosis of endothelial cells and smooth muscle cells SMCs.
By taking up ox-LDL, macrophages may transform into foam cells, which secrete growth mediators to attract SMCs into the intima. SMCs can secret extracellular matrix that forms a thin fibrous cap surrounding the fatty streak Madamanchi et al. With the continuous propagation of SMCs, monocytes, and macrophages, fatty streaks are ultimately converted into more advanced fibrous plaque Madamanchi et al.
Further, OS has also been implicated in the development cardiac hypertrophy, ischemic-reperfusion injury, and myocyte apoptosis, all of which may contribute to heart failure Madamanchi et al.
Considering the implications of ROS in CVD development, numerous studies have been performed to evaluate the effects of nutritional antioxidants in CVD patients. Consumption of fruit and vegetable is found to increase the levels of antioxidants such as carotene and vitamin C in the blood as well as decrease the cholesterol oxidation Zino et al.
Therefore, the potential benefits of fruits and vegetables in CVD have been broadly investigated. In a meta-analysis consisting of 16 prospective cohort studies andparticipants, CVD-related mortality was found to be inversely correlated with fruit and vegetable consumption Wang et al.
Another study involving patients with coronary atherosclerosis showed that supplementation of natural α-tocopherol RRR-AT can significantly reduce the incidence of CVD-related death and non-fatal myocardial infarction Table 1 Stephens et al.
However, different results are present suggesting no beneficial effect of vitamin supplementation on CVD mortality or morbidity Kris-Etherton et al.
For example, a meta-analysis study, which involved 81, participants, reported that daily supplementation of either vitamin E at a dose of 50— IU or β carotene at a dose of 15—80 mg did not decrease the mortality associated with CVD Vivekananthan et al.
Therefore, vitamin E and β carotene may not be the only active constituent of fruits and vegetables that exert cardiovascular protective effects.
Instead, other antioxidant compounds such as lycopene and polyphenols could play a more important role in the protection against CVD as will be discussed below Ignarro et al. Furthermore, the inconsistency in treatment outcomes are likely associated with antioxidant formulation. Most of the trials reporting inefficacy of vitamin E have used all-racemic α tocopherol, which is a major constituent of synthetic vitamin E Hoppe and Krennrich, ; Madamanchi et al.
By contrast, RRR-AT, the natural form of vitamin E has been associated with better treatment effects Hoppe and Krennrich, ; Madamanchi et al.
Thus, further research is needed to address the difference between RRR-AT and all-racemic α tocopherol in terms of their therapeutic efficacy. Additionally, the complicated redox mechanisms of antioxidant are far from clear now. Some of the antioxidant such as vitamin C may exhibit prooxidant properties when administrated at high doses Madamanchi et al.
This could partially explain why some of the trials using antioxidant supplementation failed to show any protective effect. Lycopene is a natural dietary antioxidant most abundant in tomatoes.
An inverse association was found between CVD incidence and consumption of either tomatoes or lycopene Kohlmeier and Hastings, ; Arab and Steck, ; Rao and Agarwal, This could be attributed to the protective effects of lycopene against LDL oxidation by inhibiting cholesterol synthesis and improving LDL degradation Table 1 Ignarro et al.
An early population-based study was conducted to evaluate the relationship between the risk of myocardial infarction and the status of three types of carotenoids including lycopene, α carotene, and β carotene, respectively. It was found that only lycopene had significant protective effects Kohlmeier et al.
Therefore, lycopene may be one of the primary contributors that underlie the protective mechanisms of vegetable consumption against CVD Kohlmeier et al. Epidemiologic studies found a significantly reduced risk for CVD with higher polyphenol intake Table 1 Vita, Beverages rich in flavonoid such as tea can markedly improve endothelial function.
However, tea consumption did not reduce the oxidative markers in the blood. So it remains elusive whether this beneficial effect of tea is elicited by its antioxidant effects Vita, Indeed, increasing evidence has suggested that the protective effects of polyphenols are not solely contributed by their antioxidant ability but more likely correlated with their anti-inflammatory effects as well as the regulation of vasodilation and apoptosis of endothelial cells Quinones et al.
Neurons are particularly vulnerable to OS-induced damage due to their weakened antioxidant defense system, high demand for oxygen consumption, and abundant polyunsaturated fatty acid content in their cell membranes Rego and Oliveira, AD is a major cause of dementia in elderly Harman, Although the exact pathogenesis of AD remains elusive, aging-related progressive increase in OS has been considered a chief contributor to the formation of AD lesions Harman, ; Pimplikar et al.
Evidence has suggested that oxidative events occur prior to the onset of plaque pathology and amyloid-β Aβ accumulation, which further supports the critical roles of OS in the initiating stage of AD Lin and Beal, ; Wang et al. OS is not the initiation factor of HD.
However, severe OS is a typical feature of HD and may contribute to the increased DNA oxidation in the HD brain Browne and Beal, OS-induced mitochondrial dysfunction is commonly observed in HD and the impairment of respiratory chain can exacerbate ROS formation Browne and Beal, Furthermore, mitochondrial aconitase, an important tricarboxylic acid TCA -cycle enzyme, is significantly impaired in HD.
The decline in aconitase activity is thought to be caused by ROS-induced oxidation of Fe-S cluster within aconitase Browne and Beal, As a result, OS is responsible for the metabolic defects seen in HD Browne and Beal, In HD, OS is also related to decreased expression of glucose transporter GLUT -3, which results in the inhibition of glucose uptake and the over-accumulation of lactate Covarrubias-Pinto et al.
: Antioxidant protection against diseases| Antioxidants: Health benefits and nutritional information | This article examines the current agzinst of redox-based therapy Antioxidant protection against diseases atherosclerosis. These Antioxidant protection against diseases are summarized Vitamin B for muscle recovery Figure 2. Evaluation Antioxidsnt salivary againsg oxidant-antioxidant status and DNA damage of children undergoing Antioxidant protection against diseases orthodontic therapy. Againsy on pathogen spectrum of 1, hospitalized children with respiratory tract infections during COVID Oxidative stress markers such as H 2 O 28-isoprostane, 8-isoprostaglandin-F2α 8-iso-PGF2α and ethane are significantly increased in the exhaled breath condensate of patients with IPF compared with healthy individuals Mitochondrial dysfunction contributes to the senescent phenotype of IPF lung fibroblasts. Both proteins can be in turn reduced back to their active form, directly by GSH or indirectly by NADPH Banafsheh and Sirous, |
| Antioxidants | Molecular mechanisms and clinical implications of reversible protein S-glutathionylation. The mechanistic links between proteasome activity, aging and age-related diseases. Cancer 69, — Under these conditions, the biological decline of the respective tissue and the reduction of the adaptive c pacity to stress appear. Hu, N. Early death A meta-analysis of 68 antioxidant supplement trials found that taking beta-carotene and vitamin A and E supplements increased the risk of dying. No use, distribution or reproduction is permitted which does not comply with these terms. |
| Main Content | Trace Elem. Reactions of manganese porphyrins with peroxynitrite and carbonate radical anion. Nworu CS, Akah PA, Okoye FB, Toukam DK, Udeh J, Esimone CO. Singh, K. Corina Amor, Inés Fernández-Maestre, … Scott W. In the early years of research in redox biology the emphasis was almost entirely on damage caused by oxidants. The level and half-life of glutathione in human plasma. |
Antioxidant protection against diseases -
Certain antioxidant vitamins, such as vitamin D, are essential in regulating biochemical pathways that lead to the proper functioning of the organs. Antioxidant supplementation has been shown to attenuate endogenous antioxidant depletion thus alleviating associated oxidative damage in some clinical research.
However, some results indicate that antioxidants exert no favorable effects on disease control. Thus, more studies are warranted to investigate the complicated interactions between ROS and different types of antioxidants for restoration of the redox balance under pathologic conditions.
This review highlights the potential roles of ROS and nutritional antioxidants in the pathogenesis of several redox imbalance-related diseases and the attenuation of oxidative stress-induced damages. Malnutrition is a poor prognostic sign in various diseases, and it is considered a major health concern in developing countries Muller and Krawinkel, Reactive oxygen species ROS are involved in many important cellular activities including gene transcription, signaling transduction, and immune response.
An overproduction of ROS can result in oxidative damage to biomolecules such as lipids, proteins, and DNA, which has been implicated in the development of aging as well as various ailments including cancer, respiratory, cardiovascular, neurodegenerative, and digestive diseases.
It is reported that the deleterious effects of excess ROS, or oxidative stress OS , eventually lead to cell death [71].
The body has equipped several mechanisms to counteract the detrimental effects of OS. Antioxidants, either endogenously generated or externally supplied, are capable of scavenging ROS and reducing the oxidation of cellular molecules, thus alleviating OS Gilgun-Sherki et al.
Antioxidants obtained from the diet are essential in supplying endogenous antioxidants for the neutralization of OS. A disturbed nutritional and redox balance is frequently observed in these patients. Malnutrition-induced antioxidant deficiency may contribute to increased risks of disease occurrence and poor treatment outcomes Ames and Wakimoto, ; Evatt et al.
Currently, the clinical awareness of nutritional balance in disease occurrence, progression, and outcomes is limited. In this review, we will outline the roles of ROS in common OS-associated diseases and aging as well as discuss the effects of nutritional antioxidants as treatments or adjuvants.
Respiratory diseases such as COPD and asthma have been identified as major health problems due to increased prevalence and mortality worldwide Masoli et al.
Environmental exposures to air pollutants and cigarette smoke contribute greatly to an increase in OS in COPD Figure 1. The toxicity of oxidants directly damages alveoli and connective tissues of the lungs, exacerbating the development of COPD van Eeden and Sin, Excessive ROS formation can also activate inflammatory cells, which in turn generate more ROS in the lungs.
This process initiates a vicious cycle of chronic inflammation and OS, as seen in COPD van Eeden and Sin, OS is also implicated in the pathophysiology of asthma Comhair and Erzurum, Although it remains inconclusive regarding whether increased OS in asthma is a causative factor of the disease or a consequence of inflammation, OS is suggested to play a pivotal role in asthma progression Cho and Moon, In bronchial asthma, OS aggravates airway inflammation by activating transcription factors such as nuclear factor-kappa B NF-κB , mitogen-activated protein kinase MAPK , activator protein-1 AP-1 , as well as pro-inflammatory mediators Figure 1.
Moreover, it enhances airway hyper-responsiveness and stimulates mucin secretion, both of which are associated with severe asthma Fitzpatrick et al. OS-induced damages in the respiratory system and the reduced antioxidant defenses further lead to an increase in endogenous ROS formation Jiang et al.
FIGURE 1. Schematic illustrating the roles of OS and nutrient antioxidants in COPD. AP-1, activator protein-1; COPD, chronic obstructive pulmonary diseases; MAPK, mitogen-activated protein kinase; OS, oxidative stress. In addition to OS, low body mass index BMI and malnutrition are suggested to correlate with the severity of COPD King et al.
Underweight COPD patients tend to experience more pulmonary damage, exercise intolerance, and increased mortality rates, in comparison to individuals with normal weights King et al. Malnutrition can lead to respiratory muscle mass reduction, which lowers the strength and endurance of these muscles Ferreira et al.
In addition, decreased intake or availability of dietary antioxidants such as vitamins C and E, carotenoids, and polyphenols, can weaken the antioxidant system and exacerbate disease progression Figure 1 and Table 1 Sies et al.
A dietary pattern that is rich in vegetables, fruits, fish, and whole grains has been associated with improved pulmonary function and a lower risk of COPD Varraso et al. It is suggested that nutritional supplementation enhances respiratory muscle function in malnourished COPD patients, thereby improving their quality of life Ferreira et al.
For example, Hornikx et al. As the most well-known nutritional antioxidant, vitamin C is capable of reducing oxidative damages and inflammation in the pulmonary system by scavenging excess ROS and activating NF-κB pathway, respectively Tecklenburg et al.
Furthermore, melatonin, a powerful antioxidant and a regulator of the sleep-wake cycle, can also attenuate OS-related lung deterioration Figure 1 and Table 1 Gumral et al. These findings support the potential use of nutritional antioxidants as an adjuvant to COPD treatment.
Similarly, several observational studies suggest that nutritional antioxidants from diets or supplements can improve asthma control and lung function in asthmatic patients Moreno-Macias and Romieu, A systematic review has proposed that there is an inverse association between dietary intake of vitamins A and C and incidence of asthma Table 1 Allen et al.
Vitamin C functions in conjunction with vitamin E to stimulate the regeneration of membrane-bound α-tocopherol from its oxidized states Moreno-Macias and Romieu, In addition, dietary carotenoids have been shown to correlate with improved asthma outcomes and lung function Wood et al.
The linkage between OS and the development of respiratory diseases suggests a pivotal role of nutritional antioxidants Romieu, Vulnerable populations include those with deficiency in dietary antioxidants, increased exposure to environmental sources of oxidants, and poor access to nutritional antioxidants Moreno-Macias and Romieu, It is important to note that although antioxidants may help to mitigate the progression of respiratory diseases, antioxidant supplements can act as pro-oxidants or OS inducers if consumed at levels that significantly surpass the recommended dietary intake Pham-Huy et al.
The potential benefits and risks of nutritional antioxidant supplementation trials in respiratory diseases should be considered on a case-by-case basis. Furthermore, it remains unknown whether OS is a consequence or the causative factor for some pulmonary diseases.
Therefore, antioxidant treatment may not be an effective approach to modify disease progression although it may be able to alleviate OS-related symptoms Margaritelis, Cardiovascular diseases CVD are the leading cause of mortality in the United States, resulting in nearly one million deaths each year Madamanchi et al.
The majority of CVD is correlated with atherosclerosis development, in which OS play a causal role Madamanchi et al. Excessive ROS can be generated in vascular cells from NAD P H oxidase Nox , nitric oxide synthases NOS uncoupling, and mitochondria, which cause oxidative modifications of low density lipoprotein LDL Azumi et al.
The oxidized LDL ox-LDL transported through the arterial lumens induces apoptosis of endothelial cells and smooth muscle cells SMCs. By taking up ox-LDL, macrophages may transform into foam cells, which secrete growth mediators to attract SMCs into the intima.
SMCs can secret extracellular matrix that forms a thin fibrous cap surrounding the fatty streak Madamanchi et al. With the continuous propagation of SMCs, monocytes, and macrophages, fatty streaks are ultimately converted into more advanced fibrous plaque Madamanchi et al. Further, OS has also been implicated in the development cardiac hypertrophy, ischemic-reperfusion injury, and myocyte apoptosis, all of which may contribute to heart failure Madamanchi et al.
Considering the implications of ROS in CVD development, numerous studies have been performed to evaluate the effects of nutritional antioxidants in CVD patients. Consumption of fruit and vegetable is found to increase the levels of antioxidants such as carotene and vitamin C in the blood as well as decrease the cholesterol oxidation Zino et al.
Therefore, the potential benefits of fruits and vegetables in CVD have been broadly investigated. In a meta-analysis consisting of 16 prospective cohort studies and , participants, CVD-related mortality was found to be inversely correlated with fruit and vegetable consumption Wang et al.
Another study involving patients with coronary atherosclerosis showed that supplementation of natural α-tocopherol RRR-AT can significantly reduce the incidence of CVD-related death and non-fatal myocardial infarction Table 1 Stephens et al.
However, different results are present suggesting no beneficial effect of vitamin supplementation on CVD mortality or morbidity Kris-Etherton et al. For example, a meta-analysis study, which involved 81, participants, reported that daily supplementation of either vitamin E at a dose of 50— IU or β carotene at a dose of 15—80 mg did not decrease the mortality associated with CVD Vivekananthan et al.
Therefore, vitamin E and β carotene may not be the only active constituent of fruits and vegetables that exert cardiovascular protective effects. Instead, other antioxidant compounds such as lycopene and polyphenols could play a more important role in the protection against CVD as will be discussed below Ignarro et al.
Furthermore, the inconsistency in treatment outcomes are likely associated with antioxidant formulation. Most of the trials reporting inefficacy of vitamin E have used all-racemic α tocopherol, which is a major constituent of synthetic vitamin E Hoppe and Krennrich, ; Madamanchi et al.
By contrast, RRR-AT, the natural form of vitamin E has been associated with better treatment effects Hoppe and Krennrich, ; Madamanchi et al.
Thus, further research is needed to address the difference between RRR-AT and all-racemic α tocopherol in terms of their therapeutic efficacy. Additionally, the complicated redox mechanisms of antioxidant are far from clear now.
Some of the antioxidant such as vitamin C may exhibit prooxidant properties when administrated at high doses Madamanchi et al. This could partially explain why some of the trials using antioxidant supplementation failed to show any protective effect.
Lycopene is a natural dietary antioxidant most abundant in tomatoes. An inverse association was found between CVD incidence and consumption of either tomatoes or lycopene Kohlmeier and Hastings, ; Arab and Steck, ; Rao and Agarwal, This could be attributed to the protective effects of lycopene against LDL oxidation by inhibiting cholesterol synthesis and improving LDL degradation Table 1 Ignarro et al.
An early population-based study was conducted to evaluate the relationship between the risk of myocardial infarction and the status of three types of carotenoids including lycopene, α carotene, and β carotene, respectively.
It was found that only lycopene had significant protective effects Kohlmeier et al. Therefore, lycopene may be one of the primary contributors that underlie the protective mechanisms of vegetable consumption against CVD Kohlmeier et al.
Epidemiologic studies found a significantly reduced risk for CVD with higher polyphenol intake Table 1 Vita, Beverages rich in flavonoid such as tea can markedly improve endothelial function.
However, tea consumption did not reduce the oxidative markers in the blood. So it remains elusive whether this beneficial effect of tea is elicited by its antioxidant effects Vita, Indeed, increasing evidence has suggested that the protective effects of polyphenols are not solely contributed by their antioxidant ability but more likely correlated with their anti-inflammatory effects as well as the regulation of vasodilation and apoptosis of endothelial cells Quinones et al.
Neurons are particularly vulnerable to OS-induced damage due to their weakened antioxidant defense system, high demand for oxygen consumption, and abundant polyunsaturated fatty acid content in their cell membranes Rego and Oliveira, AD is a major cause of dementia in elderly Harman, Although the exact pathogenesis of AD remains elusive, aging-related progressive increase in OS has been considered a chief contributor to the formation of AD lesions Harman, ; Pimplikar et al.
Evidence has suggested that oxidative events occur prior to the onset of plaque pathology and amyloid-β Aβ accumulation, which further supports the critical roles of OS in the initiating stage of AD Lin and Beal, ; Wang et al. OS is not the initiation factor of HD. However, severe OS is a typical feature of HD and may contribute to the increased DNA oxidation in the HD brain Browne and Beal, OS-induced mitochondrial dysfunction is commonly observed in HD and the impairment of respiratory chain can exacerbate ROS formation Browne and Beal, Furthermore, mitochondrial aconitase, an important tricarboxylic acid TCA -cycle enzyme, is significantly impaired in HD.
The decline in aconitase activity is thought to be caused by ROS-induced oxidation of Fe-S cluster within aconitase Browne and Beal, As a result, OS is responsible for the metabolic defects seen in HD Browne and Beal, In HD, OS is also related to decreased expression of glucose transporter GLUT -3, which results in the inhibition of glucose uptake and the over-accumulation of lactate Covarrubias-Pinto et al.
It remains inconclusive whether OS is an initiator or consequence of neurodegeneration in PD. However, excessive ROS production is a critical component of the mechanisms underlying PD progression Jenner, Loss of antioxidant defense, especially glutathione GSH content is found early in PD although the cause remains unknown Jenner, High levels of oxidation of protein, DNA, and lipids are observed in PD.
The toxic products from the oxidative damage may lead to neural cell death Jenner, In the substantia nigra pars compacta SNc of PD patients, reduced activity of Complex I in the mitochondrial respiratory chain contributes to excessive ROS generation and consequently induces the apoptosis of dopaminergic neurons Blesa et al.
In ALS, superoxide dismutase SOD 1 mutation and mitochondrial degeneration represent one of the major mechanisms underlying ALS pathology Rotunno and Bosco, Specifically, significant vacuolar degeneration of mitochondria was observed just before the death of neuron in SOD1 mutant mice, indicating that mitochondrial dysfunction initiates the onset of ALS Lin and Beal, Mutant SOD1 has been shown to abnormally interact with mitochondria, leading to cytochrome c release and activation of apoptosis Lin and Beal, A decline in antioxidant capability due to SOD1 mutation is potentially associated with motor neuron degeneration Zuo et al.
Furthermore, marked mitochondrial alterations caused by OS have been suggested to be involved in the development of SCA Stucki et al. Considering the complex roles of OS in neurodegenerative disorders, the regulation of cellular ROS levels may represent a potential treatment to impede neurodegeneration and alleviate associated symptoms Uttara et al.
Clinical evidence indicates that neurodegenerations can be ameliorated upon proper intake of natural or supplementary antioxidants Zandi et al. On the other hand, a lack of major antioxidants due to malnutrition, which is implicated in various neurodegenerative diseases, can worsen the progress of neurological conditions Brambilla et al.
For example, vitamin D deficiency has recently emerged as one of the contributing factors leading to aberrant neurological development. Vitamin D is an essential antioxidant that regulates calcium-mediated neuronal excitotoxicity and the induction of neurotransmitters and synaptic structural proteins Mpandzou et al.
Wang et al. Neurological impairments have also been manifested in individuals with a vitamin B deficiency. Multiple vitamin B e. Rutin, resveratrol, and vitamin E, which target ROS-mediated cascades such as JNK and NF-κB, have yielded some positive outcomes in improving neurodegeneration both in vitro and in vivo Zuo et al.
In a rat brain, vitamin E was found to be more effective in modulating OS than vitamins A and C Zaidi and Banu, Accordingly, a 2-year administration of vitamin E at a dose of IU per day has been shown to reduce the functional decline associated with AD Sano et al.
The combination of vitamin E and coenzyme Q10 improves energy generation in some cases of Friedreich ataxia by attenuating OS and restoring mitochondrial function Lodi et al. In addition to vitamins, phytochemicals, another type of bioactive compounds that can be found in fruits and vegetables, exhibit high antioxidant capacity with potential neuroprotective effects against PD Mazo et al.
Anthocyanin derived from strawberries possesses anti-oxidative, anti-inflammatory, and anti-apoptotic abilities. It has been reported to alleviate astrogliosis and preserve neuromuscular junctions and muscle function, serving as a possible therapeutic agent for ALS and other neurodegenerative diseases Winter et al.
Lipoic acid LA is shown to enhance GSH generation and deplete lipid peroxide, thus protecting neurons against OS-induced mitochondrial dysfunction Table 1 Moreira et al. Long-term administration of MitoQ, a mitochondria-target antioxidant, also significantly restores mitochondrial functions in Purkinje cells and alleviates SCA1-related symptoms such as motor incoordination Stucki et al.
Numerous studies have been performed to investigate the therapeutic effects of natural antioxidants on neurodegenerative disorders; however, mixed results have been yielded Dias et al.
For instance, despite the seeming effectiveness of vitamin E, a study has showed that vitamin E intake for 5 months failed to elevate vitamin E levels in ventricular cerebrospinal fluid of PD patients Pappert et al.
ROS formation is subtly regulated by antioxidant defense systems within the human body Zuo et al. Hence, single antioxidant intake could not be sufficient to resist OS under pathophysiological conditions and could result in cellular damage Murphy, In this regard, a combined use of various nutritional antioxidants should be considered.
Importantly, the simple dichotomy in redox biology comprised of good antioxidants and bad ROS is regarded as untenable.
It is now well accepted that a small amount of ROS is essential to activate redox-sensitive signaling pathways, while excessive ROS can lead to detrimental effects Margaritelis et al. The different characteristics and sources of ROS may define their specific roles in regulating cellular activities Winterbourn and Hampton, ; Margaritelis et al.
Numerous studies have stressed the need for a more precise description of the metabolism of ROS in aspects of quantity, reactivity, location, and reaction kinetics Winterbourn and Hampton, ; Forman et al.
However, most of the exogenously administrated antioxidants are non-selective and distributed uniformly across various parts of the cells or tissues Margaritelis et al. The lack of specificity of antioxidants may account for their inefficacy in treating OS-related diseases.
It is thus imperative that researchers focus on developing novel and targeted antioxidants such as mitoQ and Nox inhibitors to improve the precise therapeutic effects of antioxidants in future studies Altenhofer et al. ROS are involved in all three stages of cancer development, namely initiation, promotion, and progression Khandrika et al.
In the initiation stage, ROS-induced DNA mutations can accumulate if they are not repaired in cancerous tissues Poulsen et al. Excessive ROS production may lead to oncogenic mutation of DNA, potentially contributing to the onset of cancer Valko et al.
In addition, cancer cells are characterized by more ROS production than normal cells due to an altered metabolism and increased energy demand Sosa et al. ROS-induced OS in carcinoma cells may promote cancer growth by triggering cell growth signaling, enhancing tumor resistance to therapies, increasing blood supply to tumors, and promoting metastasis Brown and Bicknell, ROS promote the expansion of cancerous cells by modifying the genes related to apoptosis, cell proliferation and transcription factors Trueba et al.
In the progression stage of cancer development, ROS contribute to the upregulation of matrix metalloproteinases, inhibiting the action of anti-proteases and angiogenesis, eventually leading to metastasis Maulik, ; Mori et al. A depletion of endogenous antioxidants or a disruption of redox equilibrium may lead to cancer development.
Fruits and vegetables, which are rich in antioxidants, exert a protective effect against several different types of cancers Soerjomataram et al.
Plant foods that contain polyphenols have proven to be effective antioxidant agents for the body Barrajon-Catalan et al. They have been shown to possess anti-cancer activity which is effective against lung, breast, tongue, gastric, larynx, colon, and prostate cancers Table 1 Manikandan et al.
Fruits containing higher phenolic content have stronger antioxidant properties since they can induce hydroxyl group substitution in the aromatic rings of phenol compounds Sun et al.
Polyphenols induce apoptosis of cancer cells, inhibit proliferation of mutated cells, reduce production of cyclooxygenase-2 COX-2 , and downregulate cancer gene expression Gloria et al.
Moreover, nutrients such as vitamins and minerals can reduce cancer risk by eliciting antioxidant action, inhibiting proliferation of cancerous cells, maintaining DNA methylation, and promoting cell-cycle arrest Pathak et al.
In individuals previously treated for cancer, a healthy diet rich in fruits and vegetables can modify biologic markers of cancer progression Jones and Demark-Wahnefried, Healthy plant foods have shown to reduce the risk of death after being diagnosed with breast Vrieling et al.
A high vegetable diet has been shown to be effective in reducing breast cancer recurrence for patients on tamoxifen Gold et al. Vitamins such as Vitamin A and E have a preventive effect against oral cancer Garewal, However, limited evidence supports the effectiveness of vitamins and minerals in cancer prevention Fortmann et al.
Additionally, there is a lack of randomized control trials investigating diets and cancer due to difficulty in whole diet interventions as well as ethical issues in the proposed research Norat et al.
Hence, current recommendations are based on the effectiveness of a healthy diet rich in fruits, vegetables, and grains, and low on red meat and alcohol and lifestyle on reducing cancer risk Norat et al.
It is well established that intestinal inflammation-associated OS plays an essential role in the pathophysiology of various gastrointestinal GI diseases, such as inflammatory bowel diseases IBD Balmus et al. Although the exact etiology of IBD remains unclear, the underlying pathologies can be partially attributed to excess ROS formation Zhu and Li, ; Bhattacharyya et al.
Due to the presence of food particles, pathogens, or microbiota imbalance, the GI tract may become irritated, generating excess ROS and compromising endogenous antioxidant defenses Moura et al. OS disrupts the intestinal epithelial barrier and increases intestinal permeability, further exacerbating inflammation Figure 2 Balmus et al.
IBD, which is comprised of CD and ulcerative colitis UC , is characterized by chronic and prominent inflammation associated with OS in the GI tract Balmus et al.
Elevated levels of pro-inflammatory mediators such as platelet activating factor PAF and leukotriene B 4 LTB 4 observed in the mucosal samples from active IBD patients have been shown to trigger the release of cytotoxic reactive oxygen metabolites by overstimulating phagocytes Ingraham et al.
Moreover, myeloperoxidases are released during the massive infiltration of polymorphonuclear neutrophils and macrophages into the inflamed mucosa, producing hypochlorous acid, a potent oxidizing agent, via the metabolism of H 2 O 2.
Other sources of ROS include enzymes such as cyclooxygenase, xanthine oxidase, and 5-lipoxygenase that reside in the intestinal mucosa Alzoghaibi, FIGURE 2.
Schematic illustrating the roles of OS and nutrient antioxidants in IBD. IBD, inflammatory bowel diseases; OS, oxidative stress; Se, selenium; Zn, zinc. Despite ROS overproduction, a deficiency in dietary and enzymatic antioxidants also contributes to the development of OS Alzoghaibi, For example, low levels of enzymatic antioxidants and vitamins have been observed in patients with CD, which is partly due to malnutrition Buffinton and Doe, ; Alzoghaibi, In malnourished IBD patients, the reduced dietary intakes of fruits and vegetables greatly influence the concentration of carotenoid vitamin A Balmus et al.
Vitamin C, which helps to repair and protect mucosal lining against detrimental insults, is depleted in peptic ulcers and gastritis Aditi and Graham, Notably, the increased incidence of vitamin D deficiency in CD patients is highly associated with skeletal morbidity and a worsened quality of life Figure 2 van Hogezand and Hamdy, ; Alastair et al.
Persistent OS can damage the intestinal barrier and increase the permeability of GI epithelium via lipid peroxidation and tight junction disruption. This alters the composition of commensal microbiota in the GI tract and interrupts their ability to establish colonization resistance, thus promoting the invasion of pathogenic bacteria Buffie and Pamer, ; Moura et al.
Such infections further aggravate ROS production and inflammation and potentially increase the risk of inflammatory bowel syndrome Zhu and Li, Considering a strong indication of ROS elevation in IBD and other GI diseases, the adjuvant or treatment potential of antioxidants are largely investigated.
Antioxidant applications have been shown to restore redox balance, thereby attenuating intestinal damages and maintaining GI health Bhattacharyya et al. For example, studies have shown that CuZn-SOD and 5-aminosalicylic acid effectively alleviate mucosal injuries in CD by scavenging or inducing rapid decomposition of ROS Emerit et al.
In a randomized placebo-controlled study, 3 months of oral antioxidant supplementation markedly improved the serum antioxidant status in CD patients in remission. The combination of antioxidants with n -3 fatty acids further attenuated pro-inflammatory activities, thus serving as a potential treatment for CD Geerling et al.
Compared to supplements, dietary intakes of antioxidants from natural fruits and vegetables may be a safer approach to avoid overconsumption. Inappropriate antioxidant application can be harmful by scavenging of physiological ROS Bjelakovic et al. Foods rich in micronutrients such as α-tocopherol vitamin E and minerals have been reported to be beneficial in alleviating ROS damage.
For example, selenium and zinc interact with GPx and SOD, respectively, to combat OS. The combination of selenium and vitamin E has demonstrated protective effects against oxidative damage in the colon of UC rats Figure 2 and Table 1 Bitiren et al.
Several functional foods may be beneficial for IBD without undesirable effects. Free radical theory, which was first proposed by Harman in , suggests that aging is process related with progressive and irreversible accumulation of oxidative damage in the cells Harman, ; Mariani et al.
This alteration of redox profile may blunt cellular capability of buffering ROS produced both under physiological conditions and in response to external stress Kregel and Zhang, Excessive ROS accumulation can directly damage DNA, protein, and lipids, which disturbs normal cellular function Zuo et al.
Mitochondrial DNA mtDNA is particularly susceptible to OS and the mutation of mtDNA has been closely linked with the aging process Trifunovic et al. It was reported that mice with somatic mtDNA mutation exhibited an earlier onset of aging-related features such as hair loss, osteoporosis, and decreased subcutaneous fat as well as a shorter lifespan Trifunovic et al.
Exposure to high levels of ROS can also accelerate telomere shortening, which ultimately triggers cellular senescence Kregel and Zhang, For example, fibroblast cells cultured under high OS showed increased rate of telomere shortening and a reduced lifespan Vonzglinicki et al.
Additionally, aging-associated OS could be responsible for the chronic systematic inflammation as commonly seen in the elderly via the activation of NF-κB Chung et al.
NF-κB is a key regulator for inflammatory factors such as tumor necrosis factor-alpha TNF-α , interleukin IL -1β, and IL-6 Chung et al.
OS-induced NF-κB signaling is short-lived under normal conditions in contrast to chronic activation during aging Chung et al. The persistent low-level inflammation could be responsible for the development of age-related diseases such as atherosclerosis, cancer, and dementia Chung et al.
Aging population are at a higher risk of suffering from malnutrition due to a general decline in body function including decreased metabolic rate, digestive and absorptive capability Brownie, Therefore, the elderly are more likely to be affected by diseases associated with nutritional inadequacy.
For example, aging-related vitamin D deficiency has been shown to result in bone loss, susceptibility to fracture, and hyperparathyroidism Lips, Therefore, appropriate supplementation with vitamin D can reduce the risk of hip and other fractures in housebound elderly Table 1 Lips, In recent years, focus on the diet has increased due to the diet being an essential source of exogenously obtained antioxidants.
It appears that dietary antioxidants have the anti-aging activity by their ability to suppress the generation of free radicals Kandola et al. Cognitive decline represents a major health concern in aging population Kang et al. A key study by Kang et al. It was found that women who consumed more green leafy or cruciferous vegetables demonstrated the lowest cognitive decline; while fruit consumption did not affect their cognitive function Kang et al.
Interestingly, higher intake of green and yellow vegetables was also correlated with a slower rate of skin aging in Japanese women after adjustment for age, BMI, smoking status, and sun exposure Nagata et al. Energy restriction ER has recently been put up as a potential way to extend life expectancy.
This was partially due to the favorable effects of ER on redox management. Various natural antioxidants, nutraceuticals, and functional foods have been identified as free radical or progressive oxygen hunters.
Therefore, functional foods and nutraceuticals which control the antioxidant activity may represent an important role in slowing the aging process Peng et al. A diet rich in antioxidant has been shown to increase lifespan in animal models Miquel, ; Peng et al.
For instance, a diet supplemented blueberry extract was found to markedly improve the lifespan in fruit flies and Caenorhabditis elegans Wilson et al.
This was accompanied by an increased expression of SOD and catalase. The prolongevity induced by blueberry extract was not observed in SOD or catalase-mutated fruit flies. These results suggest that the beneficial effects of blueberry to extend lifespan are potentially linked with boosted endogenous antioxidant system Peng et al.
Other nutritional antioxidants including apple polyphenols, black rice anthocyanin extract, and black tea theaflavins all demonstrated prominent prolongevity effects by upregulating the endogenous antioxidant levels in animal models Table 1 Peng et al. Further research is needed to evaluate the potential effects of natural antioxidants on life expectancy in human beings.
The implication of OS in the etiology of several chronic and inflammatory diseases indicates that antioxidant-based therapy could be promising for these disorders.
Off-flavour masking of secondary lipid oxidation products by pea dextrin. Antioxidants: An Overview on the Natural and Synthetic Types. Antioxidants for vegetable oils. Intake of butylated hydroxyanisole and butylated hydroxytoluene and stomach cancer risk: results from analyses in the Netherlands Cohort Study.
High doses of synthetic antioxidants induce premature senescence in cultivated mesenchymal stem cells. Determination of synthetic phenolic antioxidants in food items using reversed-phase HPLC.
Natural Antioxidants: Function and Sources. Significance of antioxidant potential of plants and its relevance to therapeutic applications. Non-destructive assessment of flesh firmness and dietary antioxidants of greenhouse-grown tomato Solanum lycopersicum L.
at different fruit maturity stages. Antioxidants: Its medicinal and pharmacological applications. The total antioxidant content of more than foods, beverages, spices, herbs and supplements used worldwide. South African Journal of Botany Antioxidant properties, protein binding capacity and mineral contents of some plants traditionally used in the management of animal wounds.
Antioxidant and Antimicrobial Effect of Plant Essential Oils and Sambucus nigra Extract in Salmon Burgers. In vitro and in vivo antioxidant potential of milks, yoghurts, fermented milks and cheeses: a narrative review of evidence.
An overview on some of important sources of natural antioxidants. Protein hydrolysates in animal nutrition: Industrial production, bioactive peptides, and functional significance. A Review of Antioxidant Peptides Derived from Meat Muscle and By-Products.
Dietary Modulation of Oxidative Stress From Edible Insects: A Mini-Review. Functional foods enhanced with Microbial antioxidants. Antibacterial and Antioxidant Activities of Novel Actinobacteria Strain Isolated from Gulf of Khambhat, Gujarat. Lactic Acid Bacteria With Antioxidant Activities Alleviating Oxidized Oil Induced Hepatic Injury in Mice.
Oxidative stress tolerance and antioxidant capacity of lactic acid bacteria as probiotic: a systematic review. Impact of fermentation conditions on the production of bioactive compounds with anticancer, anti-inflammatory and antioxidant properties in kombucha tea extracts.
Optimal extraction, purification and antioxidant activity of total flavonoids from endophytic fungi of Conyza blinii H. Antioxidant Activity and Isolation from Soybeans Fermented with Aspergillus spp. Microalgae under environmental stress as a source of antioxidants.
Effects of Nitrogen Availability on the Antioxidant Activity and Carotenoid Content of the Microalgae Nephroselmis sp. Simultaneous accumulation of lipid and carotenoid in freshwater green microalgae Desmodesmus subspicatus LC by nutrient replete strategy under mixotrophic condition.
Metabolic Engineering of Different Microbial Hosts for Lycopene Production. Antioxidant Potential of Phycobiliproteins: Role in Anti-Aging Research. The role of antioxidants in combating the aging process. Role of antioxidants in the skin: anti-aging effects. Lycopene Deficiency in Ageing and Cardiovascular Disease.
Anti-Aging Potentials of Methylene Blue for Human Skin Longevity. Therapeutic applications of resveratrol and its derivatives on periodontitis.
Resveratrol and liver: A systematic review. Antioxidant Activity and Hepatoprotective Potential of Quercetin 7-Rhamnoside In Vitro and In Vivo.
C-Reactive Protein and High-Sensitive Cardiac Troponins Correlate with Oxidative Stress in Valvular Heart Disease Patients. Efficacy of IMOD in the treatment of oral Lichen plarius. Preclinical and phase I clinical safety of setarud IMOD a novel immunomodulator. Quercetin attenuates fasting and postprandial hyperglycemia in animal models of diabetes mellitus.
Renoprotective effect of the antioxidant curcumin: Recent findings. Effect of NCB, atorvastatin and placebo on endothelial function, oxidative stress and inflammatory markers in patients with type 2 diabetes mellitus: a randomized, parallel-group, placebo-controlled, 8-week study.
Dose escalation of a curcuminoid formulation. Potential role of green tea catechins in the management of oxidative stress-associated infertility.
Anti-inflammatory and antioxidant activities of extracts of Reissantia indica , Cissus cornifolia and Grosseria vignei. Bioavailable Citrus sinensis Extract: Polyphenolic Composition and Biological Activity.
Antioxidant and anti-inflammatory activities of extracts from Cassia alata, Eleusine indica, Eremomastax speciosa, Carica papaya and Polyscias fulva medicinal plants collected in Cameroon.
A Critical Review of Phenolic Compounds Extracted from the Bark of Woody Vascular Plants and Their Potential Biological Activity. The anti-inflammatory and antioxidant activity of 25 plant species used traditionally to treat pain in southern African.
The leaf extract of Spondias mombin L. displays an anti-inflammatory effect and suppresses inducible formation of tumor necrosis factor-α and nitric oxide NO.
Literature Review on the Biological Effects of Taraxacum officinale Plant In Therapy. Medicinal Mushrooms: Bioactive Compounds, Use, and Clinical Trials. A one-step real-time RT-PCR assay for simultaneous typing of SARS-CoV-2 mutations associated with the EK and NY spike protein amino-acid substitutions.
The isolated GTPase-activating-protein-related domain of neurofibromin-1 has a low conformational stability in solution. Assessment of Vitamin C and Antioxidant Profiles in Saliva and Serum in Patients with Periodontitis and Ischemic Heart Disease.
Sensitive Spectrophotometric Method for Determination of Vitamins C and E. Antioxidants in Oral Health and Diseases: Future Prospects. Bioactivity-guided fractionation of a methanol leaf extract from Gnetum africanum with potential anti-diabetic activity: - -epicatechin as the active principle.
Targeting oxidative stress in disease: promise and limitations of antioxidant therapy. Reference ranges for serum biochemical parameters among healthy Cameroonians to support HIV vaccine and related clinical trials. Antioxidant, Antimicrobial, and Anticancer Effects of Anacardium Plants: An Ethnopharmacological Perspective.
Antioxidant, Antimicrobial and Antiviral Properties of Herbal Materials. Berry polyphenols metabolism and impact on human gut microbiota and health.
Extraction of essential oil from Citrus reticulate Blanco peel and its antibacterial activity against Cutibacterium acnes formerly Propionibacterium acnes. Steroid Alkaloids from Holarrhena africana with Strong Activity against Trypanosoma brucei rhodesiense.
Protective Effect of Bioactivity Guided Fractions of Ziziphus jujuba Mill. Root Bark against Hepatic Injury and Chronic Inflammation via Inhibiting Inflammatory Markers and Oxidative Stress.
Phytochemicals: Extraction, Isolation, and Identification of Bioactive Compounds from Plant Extracts. Studies on pharmacology, toxicology and pharmacokinetics of the chemical constituents in hemorrheologic agent. Association analysis of biological variations in different routinely measured biochemical parameters in healthy subjects.
Spectrophotometric assay of creatinine in human serum sample. Medicinal plants with central nervous effects Part 2 : Plant based review. Measurement of GHT Glucose, Heart Rate, Temperature Using Non-Invasive Method.
Berry flavonoids and phenolics: bioavailability and evidence of protective effects. Relationship and improvement strategies between drug nanocarrier characteristics and hemocompatibility: What can we learn from the literature.
Use of graphene-based materials as carriers of bioactive agents. Copyright © Authors. This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial 4.
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Oncology Advances. Chronic Metabolic Diseases. Advanced Search. Morin suppresses the activation of NFekB on kidney models during the existence of free radicals. They improved the endogenous ROS- elimination system in mammalian tissue and helped in the possible management of skin infections and aging.
Decreases nitric oxide, ROS, and lipid peroxyl radical. Effective in stimulating skin fibroblast multiplication and delaying cellular senescence. Inhibits pro-inflammatory cytokines like IL-1 and TNF-a that are periodontitis mediators. Q7R produced hepatoprotection against CCl 4 induced hepatotoxicity and cytoprotective, antioxidant effects on H 2 O 2 treated human liver cells.
Foraged DPPH and OH radicals and stop the accumulation of ROS in neurons. They control hyperglycemia by promoting the stimulation and release of insulin. Normalized paracetamol-induced liver and kidney damage by inhibiting oxidative injury.
Reduce malondialdehyde MDA concentration and oxidative stress levels significantly. Maintenance of body function and mitochondrial redox balance.
Hepatoprotective Nephroprotective Anti-inflammatory Synergistic effects. React with superoxide anions and -OH, and is also able to chelate metal ions. Neha K, Haider MR, Pathak A, Yar MS.
Singh B, Singh JP, Kaur A, Singh N. Cevik N, Turker G, Kizilkaya B. Olas B. Ayoka T, Nwachukwu N, Nnadi C. Eboh AS. Ferdous UT, Yusof ZNB. Fang J. Alkadi H. Halliwell B. Lobo V, Patil A, Phatak A, Chandra N. Mehta SK, Gowder SJT.
Sharifi-Rad M, Anil Kumar NV, Zucca P, Varoni EM, Dini L, Panzarini E, et al. Tan SJ, Ismail IS. Ballistreri G, Fabroni S, Romeo FV, Timpanaro N, Amenta M, Rapisarda P. Messenlehner J, Hetman M, Tripp A, Wallner S, Macheroux P, Gruber K, et al. Nimse SB, Pal D. Lucas SM, Rothwell NJ, Gibson RM.
Xu DP, Li Y, Meng X, Zhou T, Zhou Y, Zheng J, et al. Anwar H, Hussain G, Mustafa I. Abbas M, Saeed F, Anjum FM, Afzaal M, Tufail T, Bashir MS, et al. Plasma lipid peroxides and alpha-tocopherol in critically ill patients.
Lyons, J. Cysteine metabolism and whole blood glutathione synthesis in septic pediatric patients. Granger, D. Role of xanthine oxidase and granulocytes in ischemia-reperfusion injury.
This article documents the sources of oxidative stress in IRI. CAS PubMed Google Scholar. Matsushima, S. Physiological and pathological functions of NADPH oxidases during myocardial ischemia-reperfusion. Trends Cardiovasc. Duilio, C. Neutrophils are primary source of O2 radicals during reperfusion after prolonged myocardial ischemia.
Heart Circ. Delanty, N. A potential quantitative marker of oxidant stress in vivo. Circulation 95 , — Reilly, M. Increased formation of the isoprostanes IPF2alpha-I and 8-epi-prostaglandin F2alpha in acute coronary angioplasty: evidence for oxidant stress during coronary reperfusion in humans.
Circulation 96 , — Seet, R. Oxidative damage in ischemic stroke revealed using multiple biomarkers. Stroke 42 , — Nagayoshi, Y.
Gong, P. Multiple basic-leucine zipper proteins regulate induction of the mouse heme oxygenase-1 gene by arsenite. Kronke, G. Expression of heme oxygenase-1 in human vascular cells is regulated by peroxisome proliferator-activated receptors. Peng, Z. Inhibitor of kappaB kinase beta regulates redox homeostasis by controlling the constitutive levels of glutathione.
Rojo, A. Mulcahy, R. This article describes an essential role for NRF2 in GSH biosynthesis. Cuadrado, A. Therapeutic targeting of the NRF2 and KEAP1 partnership in chronic diseases. Drug Discov. This article provides a comprehensive review of NRF2 as a target for therapy.
Moncada, S. Nitric oxide: physiology, pathophysiology, and pharmacology. This article provides a review of the primary role of nitric oxide in physiology and disease.
Ursini, F. Redox homeostasis: the Golden Mean of healthy living. This article examines the relationship of redox homeostasis to disease. Pickering, A. Nrf2-dependent induction of proteasome and Pa28alphabeta regulator are required for adaptation to oxidative stress.
Chowdhury, I. Oxidant stress stimulates expression of the human peroxiredoxin 6 gene by a transcriptional mechanism involving an antioxidant response element.
Rusyn, I. Expression of base excision DNA repair genes is a sensitive biomarker for in vivo detection of chemical-induced chronic oxidative stress: identification of the molecular source of radicals responsible for DNA damage by peroxisome proliferators. Cancer Res. McCord, J.
Superoxide dismutase: an enzymic function for erythrocuprein hemocuprein. Batinic-Haberle, I. Superoxide dismutase mimics: chemistry, pharmacology, and therapeutic potential. Bonetta, R. Potential therapeutic applications of MnSODs and SOD-mimetics. Chemistry 24 , — Faraggi, M.
Chemical properties of water-soluble porphyrins. Pasternack, R. Catalysis of the disproportionation of superoxide by metalloporphyrins. Peretz, P. Chemical properties of water-soluble porphyrins 3. The reaction of superoxide radicals with some metalloporphyrins.
Batinić-Haberle, I. Relationship among redox potentials, proton dissociation constants of pyrrolic nitrogens, and in vivo and in vitro superoxide dismutating activities of manganese iii and iron iii water-soluble porphyrins.
Article Google Scholar. Jaramillo, M. Manganese iii meso-tetrakis N-ethylpyridiniumyl porphyrin acts as a pro-oxidant to inhibit electron transport chain proteins, modulate bioenergetics, and enhance the response to chemotherapy in lymphoma cells. Ferrer-Sueta, G. Reactions of manganese porphyrins with peroxynitrite and carbonate radical anion.
An educational overview of the chemistry, biochemistry and therapeutic aspects of Mn porphyrins—from superoxide dismutation to H 2 O 2 -driven pathways. This article examines the potential use of SOD mimics in therapy.
Rawal, M. Manganoporphyrins increase ascorbate-induced cytotoxicity by enhancing H 2 O 2 generation. Tetrahydrobiopterin rapidly reduces the SOD mimic Mn iii ortho-tetrakis N-ethylpyridiniumyl porphyrin. Design of Mn porphyrins for treating oxidative stress injuries and their redox-based regulation of cellular transcriptional activities.
Amino Acids 42 , 95— Dorai, T. Amelioration of renal ischemia-reperfusion injury with a novel protective cocktail. Huber, W. Orgotein— bovine Cu-Zn superoxide dismutase , an anti-inflammatory protein drug: discovery, toxicology and pharmacology.
Menander-Huber, K. Orgotein superoxide dismutase : a drug for the amelioration of radiation-induced side effects. A double-blind, placebo-controlled study in patients with bladder tumours.
Sanchiz, F. Prevention of radioinduced cystitis by orgotein: a randomized study. Nielsen, O. Orgotein in radiation treatment of bladder cancer.
A report on allergic reactions and lack of radioprotective effect. Acta Oncol. Mackensen, G. Neuroprotection from delayed postischemic administration of a metalloporphyrin catalytic antioxidant. Gauter-Fleckenstein, B. Comparison of two Mn porphyrin-based mimics of superoxide dismutase in pulmonary radioprotection.
Rabbani, Z. Moeller, B. Radiation activates HIF-1 to regulate vascular radiosensitivity in tumors: role of reoxygenation, free radicals, and stress granules.
Cancer Cell 5 , — Piganelli, J. A metalloporphyrin-based superoxide dismutase mimic inhibits adoptive transfer of autoimmune diabetes by a diabetogenic T-cell clone. Diabetes 51 , — Ganesh, D. Impact of superoxide dismutase mimetic AEOL on the endothelin system of Fischer rats.
PLoS ONE 11 , e Benatar, M. Lost in translation: treatment trials in the SOD1 mouse and in human ALS. Aston, K. Computer-aided design CAD of Mn ii complexes: superoxide dismutase mimetics with catalytic activity exceeding the native enzyme.
Heer, C. Superoxide dismutase mimetic GC enhances the oxidation of pharmacological ascorbate and its anticancer effects in an H 2 O 2 -dependent manner. Antioxidants 7 , 18 Salvemini, D. Pharmacological manipulation of the inflammatory cascade by the superoxide dismutase mimetic, M Amelioration of joint disease in a rat model of collagen-induced arthritis by M, a superoxide dismutase mimetic.
Arthritis Rheum. Masini, E. Protective effects of M, a selective superoxide dismutase mimetic, in myocardial ischaemia and reperfusion injury in vivo. Anderson, C. Doctrow, S. McDonald, M. A superoxide dismutase mimetic with catalase activity EUK-8 reduces the organ injury in endotoxic shock.
This article examines the advantage of having catalase activity in SOD mimics. Xu, Y. Cardioprotection by chronic estrogen or superoxide dismutase mimetic treatment in the aged female rat. van Empel, V. EUK-8, a superoxide dismutase and catalase mimetic, reduces cardiac oxidative stress and ameliorates pressure overload-induced heart failure in the harlequin mouse mutant.
Izumi, M. Superoxide dismutase mimetics with catalase activity reduce the organ injury in hemorrhagic shock. Shock 18 , — Jung, C. Chatterjee, P. EUK reduces renal dysfunction and injury caused by oxidative and nitrosative stress of the kidney. Baker, K. Langan, A. Liu, Z. Himori, K.
PLoS ONE 12 , e Chronic antioxidant enzyme mimetic treatment differentially modulates hyperthermia-induced liver HSP70 expression with aging. Day, B. Catalase and glutathione peroxidase mimics.
Ebselen, a selenoorganic compound as glutathione peroxidase mimic. Nakamura, Y. Ebselen, a glutathione peroxidase mimetic seleno-organic compound, as a multifunctional antioxidant. Implication for inflammation-associated carcinogenesis.
Kil, J. Ebselen treatment reduces noise induced hearing loss via the mimicry and induction of glutathione peroxidase. Garland, M. The clinical drug ebselen attenuates inflammation and promotes microbiome recovery in mice after antibiotic treatment for CDI. Cell Rep. Singh, N. Effect of the putative lithium mimetic ebselen on brain myo-inositol, sleep, and emotional processing in humans.
Neuropsychopharmacology 41 , — Ogawa, A. Ebselen in acute middle cerebral artery occlusion: a placebo-controlled, double-blind clinical trial. Saito, I. Neuroprotective effect of an antioxidant, ebselen, in patients with delayed neurological deficits after aneurysmal subarachnoid hemorrhage.
Neurosurgery 42 , —; discussion — Yamaguchi, T. Ebselen in acute ischemic stroke: a placebo-controlled, double-blind clinical trial. Stroke 29 , 12—17 ICAM-1 and VCAM-1 expression induced by TNF-alpha are inhibited by a glutathione peroxidase mimic.
Castagne, V. Blum, S. Haptoglobin genotype determines myocardial infarct size in diabetic mice. Puntarulo, S. Comparison of the ability of ferric complexes to catalyze microsomal chemiluminescence, lipid peroxidation, and hydroxyl radical generation.
Brittenham, G. Efficacy of deferoxamine in preventing complications of iron overload in patients with thalassemia major.
Raftos, J. Kinetics of uptake and deacetylation of N-acetylcysteine by human erythrocytes. Rushworth, G. Existing and potential therapeutic uses for N-acetylcysteine: the need for conversion to intracellular glutathione for antioxidant benefits.
Smilkstein, M. Efficacy of oral N-acetylcysteine in the treatment of acetaminophen overdose. Analysis of the national multicenter study to Conrad, C.
Long-term treatment with oral N-acetylcysteine: affects lung function but not sputum inflammation in cystic fibrosis subjects. A phase II randomized placebo-controlled trial. Xu, R.
Effectiveness of N-acetylcysteine for the prevention of contrast-induced nephropathy: a systematic review and meta-analysis of randomized controlled trials. Heart Assoc. Wendel, A. The level and half-life of glutathione in human plasma.
Anderson, M. Glutathione monoesters. Levy, E. Transport of glutathione diethyl ester into human cells. USA 90 , — This article demonstrates that glutathione diethyl ester is highly effective as a delivery agent for GSH in human cells to decrease oxidative stress.
Puri, R. Transport of glutathione, as gamma-glutamylcysteinylglycyl ester, into liver and kidney. USA 80 , — Wellner, V. Radioprotection by glutathione ester: transport of glutathione ester into human lymphoid cells and fibroblasts.
USA 81 , — Tsan, M. Modulation of endothelial GSH concentrations: effect of exogenous GSH and GSH monoethyl ester. CAS Google Scholar. Grattagliano, I. Reperfusion injury of the liver: role of mitochondria and protection by glutathione ester.
Glutathione monoethyl ester provides neuroprotection in a rat model of stroke. Chen, T. Glutathione monoethyl ester protects against glutathione deficiencies due to aging and acetaminophen in mice.
Ageing Dev. Glutathione monoethyl ester: preparation, uptake by tissues, and conversion to glutathione. Zeevalk, G.
Howden, R. Nrf2 and cardiovascular defense. Cell Longev. Gan, L. Oxidative damage and the Nrf2-ARE pathway in neurodegenerative diseases. Acta , — Boutten, A. Protective role of Nrf2 in the lungs against oxidative airway diseases.
Google Scholar. McMahon, M. Seo, H. PLoS ONE 15 , e Lee, D. The hypertension drug, verapamil, activates Nrf2 by promoting pdependent autophagic Keap1 degradation and prevents acetaminophen-induced cytotoxicity. BMB Rep. Li, J. Green tea extract provides extensive Nrf2-independent protection against lipid accumulation and NFkappaB pro-inflammatory responses during nonalcoholic steatohepatitis in mice fed a high-fat diet.
Food Res. Pandurangan, A. Biofactors 41 , 1—14 Yagishita, Y. Broccoli or sulforaphane: is it the source or dose that matters? Molecules 24 , This article evaluates the current knowledge regarding bioavailability and efficacy of glucoraphanin and sulforaphane in terms of dose and route of administration.
Robledinos-Anton, N. Activators and inhibitors of NRF2: a review of their potential for clinical development. This article reviewed electrophilic and non-electrophilic NRF2 activators in clinical trials for various chronic diseases including cancer. Kwon, J. Sulforaphane inhibits restenosis by suppressing inflammation and the proliferation of vascular smooth muscle cells.
Atherosclerosis , 41—49 Shimizu, K. Anti-inflammatory action of curcumin and its use in the treatment of lifestyle-related diseases. de Sa Coutinho, D. Anti-inflammatory effects of resveratrol: mechanistic insights.
Jiang, Z. Discovery and development of Kelch-like ECH-associated protein 1. Nuclear factor erythroid 2-related factor 2 KEAP1:NRF2 protein-protein interaction inhibitors: achievements, challenges, and future directions.
Satoh, T. Recent advances in understanding NRF2 as a druggable target: development of pro-electrophilic and non-covalent NRF2 activators to overcome systemic side effects of electrophilic drugs like dimethyl fumarate. FRes 6 , This article evaluates NRF2 activators designed to avoid the systemic side effects caused by electrophilic activators.
Couch, R. Studies on the reactivity of CDDO, a promising new chemopreventive and chemotherapeutic agent: implications for a molecular mechanism of action. This article demonstrates that conjugation of electrophilic cyanoenone compounds and KEAP1 is selective and reversable.
Kostov, R. Pharmacokinetics and pharmacodynamics of orally administered acetylenic tricyclic bis cyanoenone , a highly potent Nrf2 activator with a reversible covalent mode of action.
Dinkova-Kostova, A. An exceptionally potent inducer of cytoprotective enzymes: elucidation of the structural features that determine inducer potency and reactivity with Keap1. Sedlak, T. Sulforaphane augments glutathione and influences brain metabolites in human subjects: a clinical pilot study.
Neuropsychiatry 3 , — PubMed PubMed Central Google Scholar. Wise, R. Lack of effect of oral sulforaphane administration on Nrf2 expression in COPD: a randomized, double-blind, placebo controlled trial. Greaney, A. Sulforaphane inhibits multiple inflammasomes through an Nrf2-independent mechanism.
Roy, S. Satoh, H. Nrf2 prevents initiation but accelerates progression through the Kras signaling pathway during lung carcinogenesis. This article demonstrates that NRF2-deficient mice exhibited an increase in tumour foci after urethane induction but a reduction in tumours with more malignant characteristics.
Wiel, C. BACH1 stabilization by antioxidants stimulates lung cancer metastasis. Cell , — e This article demonstrates that long-term supplementation with N -acetylcysteine and vitamin E promoted KRAS-driven lung cancer metastasis, and NRF2 inhibitor BACH1 stimulated glycolysis-dependent lung cancer metastasis in a mouse model.
Tao, S. The effects of NRF2 modulation on the initiation and progression of chemically and genetically induced lung cancer. This article demonstrates that sulforaphane prevented the initiation of vinyl carbamate-induced lung cancer in mouse models but promoted the progression of pre-existing tumours.
Shibata, T. Genetic alteration of Keap1 confers constitutive Nrf2 activation and resistance to chemotherapy in gallbladder cancer.
Gastroenterology , — Homma, S. Nrf2 enhances cell proliferation and resistance to anticancer drugs in human lung cancer. Jiang, T. High levels of Nrf2 determine chemoresistance in type II endometrial cancer.
Roh, J. Nrf2 inhibition reverses the resistance of cisplatin-resistant head and neck cancer cells to artesunate-induced ferroptosis.
Sporn, M. NRF2 and cancer: the good, the bad and the importance of context. Cancer 12 , — Milkovic, L. Controversy about pharmacological modulation of Nrf2 for cancer therapy. Wu, S. Nrf2 in cancers: a double-edged sword. Cancer Med. Massart, C.
Diphenyleneiodonium, an inhibitor of NOXes and DUOXes, is also an iodide-specific transporter. FEBS Open Bio. Augsburger, F. Pharmacological characterization of the seven human NOX isoforms and their inhibitors. Teixeira, G. Cifuentes-Pagano, M.
Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage. Nature , — This article demonstrates that prevention of mitochondrial superoxide production blocked oxidative stress and signal transduction. Detaille, D. An old medicine as a new drug to prevent mitochondrial complex I from producing oxygen radicals.
PLoS ONE 14 , e Craven, R. SOD mimetics to the rescue. Pavon, N. Ebselen induces mitochondrial permeability transition because of its interaction with adenine nucleotide translocase.
Murphy, M. Targeting lipophilic cations to mitochondria. Li, Y. New developments and novel therapeutic perspectives for vitamin C. Frei, B. Ascorbate is an outstanding antioxidant in human blood plasma. USA 86 , — Buettner, G.
The pecking order of free radicals and antioxidants: lipid peroxidation, α-tocopherol, and ascorbate. Bruno, R. Faster plasma vitamin E disappearance in smokers is normalized by vitamin C supplementation.
Hill, K. Combined deficiency of vitamins E and C causes paralysis and death in guinea pigs. Traber, M. Vitamin E, antioxidant and nothing more. Maxfield, L.
Vitamin C Deficiency. Vitamin E inadequacy in humans: causes and consequences. Fang, Y. Free radicals, antioxidants, and nutrition. Nutrition 18 , — Sayin, V. Antioxidants accelerate lung cancer progression in mice. Transl Med. This article demonstrates that N -acetylcysteine and vitamin E markedly increased tumour progression and reduced survival in mouse models of lung cancer.
Le Gal, K.
Antioxidant protection against diseases stress plays an essential Antioxiddant Antioxidant protection against diseases the pathogenesis of chronic Muscle building nutrition such as cardiovascular diseases, Antioxidaht, neurodegenerative diseases, and cancer. Long term exposure to increased againsy of pro-oxidant factors Antipxidant cause structural agaiinst at a mitochondrial DNA level, as well as functional alteration of several enzymes and Antioxidant protection against diseases structures leading to aberrations in gene expression. Protecgion modern lifestyle associated with processed food, exposure to a wide range of chemicals and lack of exercise plays an important role in oxidative stress induction. However, the use of medicinal plants with antioxidant properties has been exploited for their ability to treat or prevent several human pathologies in which oxidative stress seems to be one of the causes. In this review we discuss the diseases in which oxidative stress is one of the triggers and the plant-derived antioxidant compounds with their mechanisms of antioxidant defenses that can help in the prevention of these diseases. Finally, both the beneficial and detrimental effects of antioxidant molecules that are used to reduce oxidative stress in several human conditions are discussed. Many natural biological processes in our bodies, such as breathing, digesting food, metabolize alcohol and drugs, and turning fats into energy produce harmful compounds called free radicals. Thank you for visiting nature. You Functional fitness training using a browser version with limited support protectin CSS. Antioxidant protection against diseases obtain Antioxidang best experience, Antioxidaant Antioxidant protection against diseases you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. An Author Correction to this article was published on 13 July
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