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Oxidative Stress and Brain Health and HealingPreventing oxidative stress -
Is your body under attack from oxidative stress? Chances are good that it is — oxidative stress is a natural phenomenon that occurs when your body cells, tissues, and organs perform their everyday functions. The bad news is that excessive oxidative stress can lead to early aging and poor health, affecting your overall wellness.
Fortunately, you can take steps to reduce oxidative stress and combat its effects on your body. The first step in reducing oxidative stress is to understand it.
Many body cells, tissues, and organs work by breaking down molecules into atoms. Each atom has several electrons, which are particles that carry a negative charge. Some electrons, known as valence electrons, like to bond to create new, more stable atoms and molecules.
These electrons can be transferred from one atom to another, shared between neighboring atoms, or shared with all the atoms in a material. Electrons like to bond in pairs — which gives them stability.
Unpaired electrons, known as free radicals, are unstable. Free radicals seek out other unpaired electrons they can bond with or steal. While bonding makes free radicals more stable, it changes how the molecule works.
How molecules work changes how cells, tissues, and organs work. Stealing electrons also causes instability in the atoms that give up their electrons. The newly-created free radicals also scavenge for available electrons, and as they do so, create even more free radicals.
This chain reaction can damage cell membranes and DNA , alter chemical reactions in the body, and damage connective tissue and collagen. Free radicals are a byproduct of everyday physiological functions and as the result of exposure to X-rays, ozone, cigarette smoke, industrial chemicals, air pollutants, and other external sources.
The most common source of free radicals is oxygen — specifically when the body cells break down oxygen to use as energy in a process known as oxidation. Breaking down the oxygen can cause oxygen atoms to lose electrons and create free radicals.
The body fights this imbalance with antioxidants, natural substances that can provide free radicals with electrons without becoming unstable. Your body cells produce some antioxidants, but you also get antioxidants through some of the food you eat.
Oxidative stress is a condition in which you have more free radicals than antioxidants. Laboratory testing can measure antioxidant levels in your blood.
The damage caused by oxidative stress can cause a wide variety of diseases and health concerns, such as:. Oxidative stress can cause widespread damage to your cells, protein, and DNA. The damage oxidative stress causes can accelerate the aging process.
Blueberries, strawberries, and cranberries are all high in antioxidants, as are broccoli, spinach, potatoes, and carrots. These foods promote oxidation in their own way. For example, exposure to sunlight, air, or heat can cause oxidation in dietary fats and oils.
Cells break down sugar to use as fuel, and in the process, it causes oxidation. The preservatives in processed foods may create free radicals. Quit smoking, limit alcohol consumption, and exercise regularly.
To increase the energy available to your stressed-out cells, your breathing rate increases, as does the rate at which your cells break down sugar — both can cause free radicals and oxidative stress.
Research also suggests that free radicals may be beneficial in the process of wound healing. However, because free radicals have an uneven number of electrons, they are more reactive. Exposure to an excessive amount of free radicals causes oxidative stress in your body.
This can happen because of:. Oxidative stress may lead to adverse health effects such as:. Your body naturally produces some free radicals in response to exercise or certain food or drink. For example, drinking alcohol can cause an increase in free radicals.
Cumulative exposure to free radicals from these sources can lead to oxidative stress and cause cell and tissue damage. Lifestyle factors that can increase oxidative stress, such as sun exposure and smoking, may also cause skin damage.
Since antioxidants fight free radicals, some experts consider an antioxidant-rich diet helpful in defending against oxidative stress.
Studies are mixed on whether supplementing with antioxidants is an effective way to fight oxidative stress. C60 is an example of a supplement that may provide antioxidant benefits. That said, more research on the potential benefits and risks of taking supplements is needed.
Talk with your doctor to find out if supplements are right for you. Though your body needs some free radicals to function, exposure to high levels through your environment and lifestyle choices can lead to oxidative stress, potentially causing damage and disease.
Ways to help defend your body against oxidative stress include exercising, sleeping enough, reducing stress, limiting alcohol consumption, quitting smoking, and eating a healthy diet high in antioxidant-rich foods.
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and the Preventingg oxidases Preventibg catalyse reaction 2 refsPreventing oxidative stress, :. The rate of H Prevetning O 2 oxidativf largely determines whether redox signalling, etress stress or no significant oxidation occurs.
H 2 O 2 is reduced enzymatically by 15 enzymes, including catalase reaction 4 :. the five peroxiredoxins that use thioredoxin a small protein with two crucial cysteines, Trx SH 2 or the eight glutathione peroxidases and peroxiredoxin 6 that use the tripeptide, glutathione γ-glutamyl-cysteinyl-glycine, GSH reactions 5 and 6 :.
H 2 O 2 does not easily oxidize most molecules but it can react rapidly with transition metals such as iron to produce hydroxyl radical reaction 7, often referred to as the Fenton reaction :. The hydroxyl radical is an extraordinarily strong oxidant that will rapidly oxidize whatever molecule it is next to.
where LH is a lipid with allylic hydrogens, which are present in polyunsaturated fatty acids including arachidonic acid. Superoxide can cause release of iron from iron—sulfur proteins, which can then catalyse reaction 7. Peroxynitrous acid is a very strong oxidant that has the reactivity of the intermediates formed in its decomposition reaction 12 :.
The final oxidants we consider are the hypohalous acids HOX that are formed from H 2 O 2 in reaction 13, which is catalysed by phagocytic cell myeloperoxidases:.
They play a major role in tissue damage associated with phagocyte-mediated inflammation. There are two major mechanisms through which oxidative stress contributes to disease. The second mechanism of oxidative stress is aberrant redox signalling Box 2.
Oxidants, particularly H 2 O 2 generated by cells upon physiological stimulation, can act as second messengers 8. In oxidative stress, non-physiological production of H 2 O 2 can cause redox signalling to go awry 4. Both types of oxidative stress mechanism can occur in a single disease, such as in diabetes, where both advanced glycation products accumulate and aberrant activation of stress signalling pathways leads to diabetic complications 9.
Oxidative stress has been associated with a wide range of pathologies. On the basis of the contribution of oxidative stress to the aetiology of these pathologies, they have been grouped into two categories below: first, oxidative stress as the primary cause of pathology including toxicities caused by radiation and paraquat, and in atherosclerosis ; second, oxidative stress as the secondary contributor to disease progression such as in COPD, hypertension and Alzheimer disease.
However, as the role of oxidative stress in many diseases is incompletely understood, this categorization is tentative. Redox signalling is dependent on specific interactions of signalling proteins with hydrogen peroxide H 2 O 2 or other electrophiles that act as second messengers.
As with oxidative stress, both endogenous and exogenous sources of H 2 O 2 or other electrophiles may be involved; however, for redox signalling to be physiological rather than pathological, regulation is essential and requires the involvement of specificity that is not part of oxidative stress.
Maintaining redox homeostasis is important for cell function. Despite its name, homeostasis does not imply that nothing is changing. Indeed, a balance between oxidants and reductants, including glutathione, thioredoxin and NADPH, which are the substrates for antioxidant enzymes, is essential for maintaining normal physiology Thus, diseases that involve oxidative stress can be due to disruption of redox homeostasis, with type 2 diabetes mellitus as one example 9.
Adaptive homeostasis, as defined by Kelvin Daviesinvolves elevated antioxidant defences brought about by transient alteration of redox homeostasis and redox signalling. However, redox signalling may also occur under pathological conditions, as oxidative stress can stimulate the same pathways as redox signalling under physiological conditions.
The difference in this context is that the signalling will be unregulated and accompanied by nonspecific damage. It is not a perfect system as evidenced by a low rate of oxidized proteins that accumulate with age.
Oxidative stress can be a primary factor in toxicity and disease. However, an important caveat is that once damage begins, antioxidant therapy often fails to inhibit the progression of tissue injury as other factors become dominant in the pathology. Early pneumonitis followed by fibrosis frequently occur as side effects of radiotherapy for lung and oesophageal cancers Over a longer period, aberrant redox signalling for the continuous production of cytokines causes accumulation of collagen and lung fibrosis Oxidative stress is also responsible for the toxicity of the widely used chemical herbicide, paraquat.
When ingested, paraquat is actively taken up by alveolar type II cells and leads to pneumonitis and progressive lung fibrosis with poor prognosis. Paraquat also causes injury to other organs including liver and kidney. Long-term exposure to paraquat is associated with Parkinson disease In atherosclerosis, plaque builds up in the intimal layer of arteries and over time the arteries narrow, leading to infarction and stroke.
Substantial evidence indicates that oxidative stress has a crucial role in the pathogenesis of atherosclerosis. Since the first identification of lipid hydroperoxides in human atherosclerotic aorta 18many studies have shown an increase in oxidized lipids and other oxidative stress markers in the atherosclerotic lesions.
Furthermore, isoprostanes, peroxidation products of arachidonic acid, have been reported to be increased at least fivefold in human atherosclerotic lesions compared with human umbilical veins, and oxidized linoleic acid was detected only in human lesions In many diseases, oxidative stress occurs secondary to the initiation of pathology by other factors.
Oxidative stress can disturb various signalling pathways and affect multiple biological processes through modifying proteins, promoting inflammation, inducing apoptosis, deregulating autophagyimpairing mitochondrial function and many other mechanisms.
These effects frequently accelerate pathological progression and exacerbate the symptoms of diseases, as discussed in representative examples below. Cigarette smoking, the main cause of COPD, is an abundant source of oxidants. Oxidative stress can lead to oxidation and inhibition of α1-antitrypsin, thus reducing its ability to inhibit neutrophil elastase, a major factor in the pathogenesis of COPD In addition, chronic exposure to oxidants in cigarette smoke causes and promotes the inflammatory response and other pathological cascades such as cell death and fibrosis in COPD pathogenesis The sources of oxidants in COPD are both exogenous for example, cigarette smoking and air pollution and endogenous for example, NOX, mitochondria, inducible nitric oxide synthase iNOS and myeloperoxidase Increased levels of oxidants and lipid peroxidation products, including 8-isoprostane, have been consistently detected in exhaled breath condensate of patients with COPD compared with healthy controls The level of oxidative stress was inversely correlated with lung function of the patients Together, these results suggest that oxidative stress occurs both in the lung and systemically in patients with COPD and contributes to disease pathogenesis.
The pathology of idiopathic pulmonary fibrosis IPF is characterized by diffuse and progressive mesenchymal fibrosis and mild inflammation in the lung with unknown aetiology. Many studies have shown the presence of oxidative stress in IPF. 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 In addition, 8-isoprostane is elevated fivefold 28 and oxidized proteins twofold 29 in bronchoalveolar lavage fluid BALF of patients with IPF.
HNE in lung 30 and 8-isoprostane in blood 31 are also significantly elevated in IPF. The glutathione GSH level in epithelial lining fluid and sputum of patients with IPF is fourfold lower than in healthy controls 32indicating a deficiency of this important component of antioxidant defence in IPF.
H 2 O 2 production is apparently mainly from NOX4 ref. Mounting evidence suggests that oxidative stress plays a significant part in IPF, by promoting fibrogenesis through causing apoptosis of alveolar epithelial cells, activating myofibroblasts and inducing an inflammatory response Besides oxidative stress, IPF pathogenesis involves a number of processes including apoptosis, senescence, epithelial—mesenchymal transition, endothelial—mesenchymal transition, epithelial cell migration, increased production of chemokines, cytokines and growth factors, as well as mitochondrial dysfunction, endoplasmic reticulum stress, hypoxia and inflammation These mechanisms are interrelated, with oxidative stress representing an important component of the IPF pathogenesis.
Multiple risk factors such as diet, smoking, lifestyle, genetics and comorbidities contribute to hypertension. At the molecular level, however, oxidative stress is a common feature of this condition. Experimental studies suggest that oxidants are mainly from NOXs in hypertension Oxidative markers, including H 2 O 2 ref.
H 2 O 2 has a role in the development and progression of hypertension, through influencing angiotensin II signalling, NO signalling and other cellular processes However, a causative role of oxidative stress in hypertension has not yet been established.
Patients with type 2 diabetes mellitus display substantial evidence of oxidative stress that results in microvascular and macrovascular complications Markers of oxidative stress, including OxLDL to LDL ratio 448-OHdG 458-iso-PGF2α 46protein carbonyls 47 and GSH conjugation to haemoglobin 48have been reported to be significantly elevated in the plasma of patients with type 2 diabetes mellitus, as have urine 8-OHdG and 8-iso-PGF2α levels
: Preventing oxidative stress| Publication types | Redon, J. Diaphragmatic breathing reduces Preventing oxidative stress oxidative Preventing oxidative stress. The following srress Preventing oxidative stress with antioxidant activity and the foods Muscle preservation during weight loss which oxidatiive are found:. Chemical properties of water-soluble porphyrins 3. Experimental studies suggest that oxidants are mainly from NOXs in hypertension Oxidative damage is at the root of diseases including: Some types of cancer Diabetes Cardiovascular disease Multiple sclerosis It plays a role in the biological ageing process. |
| Strategies for reducing or preventing the generation of oxidative stress | Pregenting neutralizing effect of antioxidants helps Prevehting the Preventing oxidative stress from oxidative Herbal medicine for skin conditions. Stress and Trauma: PPreventing Science Behind It, How It Shows Up Preventing oxidative stress How to Heal: Dr. Recent Podcasts. A Oidative for Teens Are You a Workaholic? Preventjng is making you susceptible to HPV? Why Parkinson's research is zooming in on the gut Tools General Health Drugs A-Z Health Hubs Health Tools Find a Doctor BMI Calculators and Charts Blood Pressure Chart: Ranges and Guide Breast Cancer: Self-Examination Guide Sleep Calculator Quizzes RA Myths vs Facts Type 2 Diabetes: Managing Blood Sugar Ankylosing Spondylitis Pain: Fact or Fiction Connect About Medical News Today Who We Are Our Editorial Process Content Integrity Conscious Language Newsletters Sign Up Follow Us. Polyphenols and vitamin C are examples of water-soluble antioxidants. |
| How Breathing Exercises Balance the Impact of Intensive Training | For example, patients with non-small-cell lung cancer have Preventng shown oxieative exhale more H 2 O 2 than control stresa Preventing oxidative stress, M. Neurology 94 Preventing oxidative stress, e—e The reaction of NO with superoxide. Through aberrantly altering signalling transduction pathways that damage DNA and exacerbate inflammation, oxidants are involved in various phases of tumorigenesis, including transformation of normal cells to tumour cells, tumour cell growth, proliferation, invasion, angiogenesis and metastasis In the right amount, they are crucial to maintaining human health. |
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