Free radicals and cellular aging -
If the limits of adaptive response to a stimulus are exceeded, or when the adjustment is impossible, a series of events occur, causing cell damage, which is reversible up to a limit, but if the stimulus is intense or continued from the beginning the cell reaches a point of no return and suffer irreversible injury followed by cell death.
Pollard and Earnshaw describe that the accidental cell death, known as necrosis, occurs when a cell receives an ill chemical that causes structural or irreparable damage. Its main feature is the fact that the cells die because they are damaged and disintegrated and digested by its own lytic enzymes.
An initial cell death feature is the accidental loss of the plasma membrane integrity, so that there is an excessive influx of water in the cell, which swells until the cell membrane and the organelles break and thus the cell auto-digest and launches their cytoplasmic contents to the extracellular environment.
This action causes a local inflammation by the accumulation of phagocytic cells that are activated by the ingestion of cellular debris, and usually involves large groups of neighboring cells Pollard and Earnshaw, The increase of ROS levels can lead to necrosis by causing the transition of mitochondrial permeability, disabling the power and recovery of cellular ATP.
The ischemia may affect the antioxidant defense mechanisms of the cells accumulating free radicals by producing superoxide anions due to indirect and incomplete reduction of oxygen by amended mitochondria, or by the action of leukocytes oxidase and parenchymal cells Freitas et al.
Another type of cell death is by apoptosis silent cell death , designed to remove the unwanted cells from the host by activation of internally programmed events, those made by a group of gene products. The cell apoptosis occurs during the development, as a defense mechanism, a homeostatic process, which keeps the cells in tissues when they are damaged by pests, diseases or the aging process Cotran et al.
According to Alberts et al. There is surface bubbles formation in the fragmentation, forming apoptotic bodies which are phagocytized and replaced by the adjacent cells, occupying the space that migrate out of the cell. Solá et al. According to these authors, the cells committed to apoptotic cell death remain under inactive pro-forms, called latent phase, until the activation of apoptotic process which occurs by proteolytic cleavage that makes the starting caspase activation, triggering the executing caspase.
This cleaves a variety of essential proteins and substrates for cellular life, entering then the implementation phase.
According to Pollard and Earnshaw , during this stage the cells undergo the morphological and physiological changes, leading to death. Silva and Silva reported that some studies showed that the action of ROS induced to apoptotic cell death during the aging process, because they caused changes in proteins, DNA and telomere.
Horta and Young stated that both the excess and apoptotic failure affected the vital organic processes that could generate the diseases, which, according to Harman varied with each person due to genetic differences and exposure to certain environmental factors.
Exposure to small doses of hydrogen peroxide or the accumulation of ROS by the reduction of glutathione induce to apoptosis in uncontrolled cell fungi, a fact indicating that the ROS are key regulators of apoptosis in this organism Madeo et al.
According to Solá et al. Salvador et al. Baynes points out that other potential mechanisms may increase the power of oxidative stress in diabetes: the autoxidative glycosylation, the polyol pathway in the macroangiopathy related to hypoxia and changes in levels of inflammatory mediators.
In atherosclerosis, chronic-degenerative disease that leads to blockage of arteries by accumulation of lipids in their walls Carvalho Filho and Alencar, ; Papaléo Netto et al.
Besides these factors, there is also the influence of reactive species in the development of this pathology. According to Wink and Mitchell , the influence of nitric oxide in the genesis of atherosclerosis seems to be related to an environment rich in superoxide, which in the presence of peroxidases or superoxide, nitric oxide reacts rapidly to produce a variety of nitrogen reactive species NRA.
Carr et al. Another diseases that can be triggered by the action of free radicals are a benign and a malignant neoplasm Salvador et al. Silva and Silva describe that neoplasia comes from the changes in the apoptotic process, or even in cell proliferation caused heterostasis, or a leak of temporary equilibrium, which favors the accumulation of disorderly cells in a tumor causing symptoms that characterize the cancer, which, according to Malzyner and Caponero , incidence increases with age.
According to Salvador et al. Silva and Silva emphasize that the injury to the DNA molecule, especially in the genes mutation that control the proliferation of normal cells, results in homeostasis loss of tissue and disruption of the normal cellular events.
The non-transmissible chronic diseases of a neurological order such as Parkinson's, Alzheimer's disease and amyotrophic lateral sclerosis, may also have their origin connected with the action of oxidative stress Salvador et al. According to Pearce et al. Both records can lead and increase the generation of free radicals such as hydrogen peroxide and hydroxyl radical.
High levels of lipids peroxidation and catalase enzymes, superoxide dismutase and glutathione peroxidase were found in various regions of the brain of individuals with Alzheimer's Pappolla et al. Moreover, high levels of 8-hydro-deoxyguanosine 8-OHdG , a mutagenic product produced in DNA by different ROS, and nitrotyrosine, an oxidated amino acid were also evidenced Nunomura et al.
In relation to amyotrophic lateral sclerosis, Pedersen et al. The presence of enzymes that degrade the nucleotides, ATP, ADP and AMP in non-transferable chronic diseases of neurological order indicate the involvement of oxidative stress in the genesis of the disease, since the brain consumes high amounts of oxygen and is susceptible to the oxidative stress because the metabolism of neurotransmitters such as glutamate and dopamine, which generates ROS, consume the antioxidant defenses, causing lipid peroxidation of neuronal membranes as well as changes in cellular homeostasis Salvador et al.
There are differences regarding the extent of life and the pace of aging, considering that the maximum life duration is immutable and aging rate is unalterable. However, some researchers do not agree with this. Papaléo Netto and Borgonovi reported that some factors influenced the aging process delaying it.
Cotran et al. The cell posseses an antioxidant defense system to protect itself Ferreira and Matsubara, Novelli suggests that there are two basic lines of antioxidants: the antioxidant enzymes, which correspond to enzymes of the glutathione, catalase and peroxide dismutase, and those non-enzymatic antioxidants, such as certain types of vitamins such as ascorbic acid and tocopherol, and endogenous components such as bilirubin.
Ferreira and Matsubara subdivided these lines into two groups. The first, with and detox action by agents, acting before they cause any harm, being composed by the enzymes superoxide dismutase, catalase, glutathione peroxidase and vitamin E.
And the second group that repairs the injury occurred, is composed by the enzymes glutathione reductase and glutathione peroxidase and ascorbic acid.
Table 2 presents the main enzymes that act in the biological processes against the cell oxidative damage.
According to Baynes , the oxidative stress is increased not only by high production of precursors of ROS, but may also be emphasized by low efficiency of enzymatic systems that control them.
However, this can be prevented if certain measures are taken. There is clear concern to establish a preventive measure to mitigate or combat the organic changes promoted by the oxidative stress in aging Aranha et al.
According to Faine et al. However, this influence is not yet fully established. Despite extensive investigations, the effects of calorie restriction have not been analyzed according to the amount and type of nutrient present in the diet.
It's convenient to remember that great part of the population, in an attempt to reduce the food intake, restricts the amount of food ingested, forgetting of the diet components qualify Diniz et al. Due to the possible relation among dietary restriction, oxidative stress and cardiovascular disorders, the study of the effects of the caloric restriction on lipid rich diets is very important, since this kind of diet has many effects on heart tissue, as long as the type of fatty acid present on the diet is related to the composition of phospholipids on myocardium cell membranes Diniz et al.
In general, the consumption of the diets rich in fatty acids with double links change the content of membrane fatty acids, favoring the presence of unsaturated lipids and increasing the susceptibility to lipoperoxidation.
Some flavonoids, the flavonols, flavones and catechins, found in the fruits, vegetables, whole grains and grasses, have been also used in medicine against osteoporosis and inflammation, because they inhibit the precaution of the prostaglandin, diminishing the synthesis of nitric oxid, having a very important antioxidant characteristic Bianchi and Antunes, ; Novelli Filho and Novelli, Fernandes et al.
Diniz et al. Gomes et al. According to Aranha et al. It can be found in the foods such as the citrus citric fruits, tomatoes, strawberries, sweet-peppers and broccoli. Studies by Bianchi and Antunes showed a protective role of the vitamin in preventing the development of tumors.
However, its recommendation should be specific to each case, because the organic and inorganic components of the cell can affect its antioxidant action.
In the experiments with diabetic rats, Zanoni et al. It was likely that this reduction happened due to the oxidative stress, which promoted an increase on the free radicals frequency and a decrease on the substances responsible for fighting them, the antioxidants.
The tissue concentrations of ascorbic acid also reduced because its transport was inhibited during hyperglycaemia. Vitamin E can be found in the vegetable oils in varying forms; such as G-tocopherol, D-tocopherol, B-tocopherol and A-tocopherol the latter is a form of antioxidants widely distributed in the tissues and plasma.
These vitamins prevent the spread of reaction induced by the free radicals on the biological membrane minimizing the damage associated with the cancer, arthritis and aging Bianchi and Antunes, Spada and Silva described that the carotenoids were the precursor of vitamin A, the most important being B-carotene, found in spinach, carrots, pumpkin, mango, papaya and beets.
Vitamin A may have an antioxidant or pro-oxidant role, because the carotenoids influence the singlet oxygen, inhibiting lipid peroxidation and sweeping the free radicals. However, under high oxygen pressure, they lose their antioxidant activity.
The use of minerals, such as zinc and selenium, with an antioxidant role, is linked to the dependence of antioxidant enzymes by these minerals.
The superoxide dismutase depends on copper and zinc and the gluthathione dismutase on selenium. The reduced levels of this minerals results in susceptibility to oxidative damage on the cells and promotes the process of carcinogenesis Bianchi and Antunes, These minerals establish an indirect action.
As an antioxidant, zinc regulates the expression of methollothioneins and protection of sulfhydryl groups of membrane proteins Koury and Donangelo, According to Kehl and Cassini , the physical activity has been able to mitigate the risk of many diseases.
Burneiko et al. Thus, physical exercises decreases, for example, the risk of cardiovascular disorders, because it normalizes the lipid profile, promoting the fat oxidation and reducing the deleterious effects of the hypercaloric diet. In contrast, as the mitochondrial oxygen flow should be high for the production of ATP during the exercise, the increase of the production of ROS may occur, which could lead to oxidative damage.
The same way, changes in the diet components, like the substracts to obtain energy, are also associated to oxidative stress Burneiko et al. The imposition made by modern lifestyle that limits the time spent on feeding results in the ingestion of varying caloric content diets and the practice of physical exercises of different intensities Schneider and Oliveira, To evaluate the resistance to exercise, the improvement of lipid profile and weight loss, the effect of different types of diets associated with physical activity have been subject of several and frequent studies.
However, the effects of the interaction between the hipercaloric diet intake and practice of physical exercises in oxidative stress and energy metabolism have not been well established. A balanced diet coupled with daily exercise promotes the beneficial effects, reducing the lipid serum profile and the myocardic lipid peroxidation.
On the other hand, a hypercaloric diet associated with inactivity leads to dyslipidemia, which can be normalized by the exercise. When physical exercise is performed daily, the normalization of the serum lipid profile is obtained even when associated to hypercaloric diet, although, in this condition, increase of mycordial lipid peroxidation occurs Schneider and Oliveira, There are many theories that attempt to explain the mechanisms involved in the biological aging.
However, none of them provide full and definite reasons for the development of such phenomenon. The tests performed with non-enzymatic antioxidants vitamins A, E, C, flavonoids, carotenoids and minerals and calorie restriction and physical exercises had been proved as beneficial alternatives to reduce, protect, and prevent the expansion of biomolecules oxidative damages and cell aging.
Just like bodily systems balanced and coordinated interrelationship, the theory of oxidative stress, the focus of this work, and other existing theories shouldn't be evaluated in isolation but in a broader context because, despite the variety of mechanisms mentioned, all the strategies have not been proved yet.
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The free radical cellulae of aging states that agingg age because cells accumulate free Sports nutrition guidelines for vegetarian and vegan athletes damage over time. Ahd are reducing Free radicals and cellular agingand limit oxidative damage to radlcals structures by Free radicals and cellular aging them from free radicals. Denham Agign first proposed the free radical theory of aging in the s, [5] and in the s extended the idea to implicate mitochondrial production of ROS. In some model organisms, such as yeast and Drosophilathere is evidence that reducing oxidative damage can extend lifespan. The free radical theory of aging was conceived by Denham Harman in the s, when prevailing scientific opinion held that free radicals were too unstable to exist in biological systems.Video
Free Radicals Explained Simply - Medical Animation Aging is an inevitable biological process, characterized snd a general decline in physiological and biochemical functions of Free radicals and cellular aging celllular systems. In the case of the neuromuscular system, adn in nad and mobility Healthy and Refreshing Snack Options a deterioration Free radicals and cellular aging motor performance, impaired mobility, and disability. At the cellulra level, aging is caused by a progressive decline in mitochondrial function that results in accumulation of reactive oxygen species ROS. As the level of oxidative stress in skeletal muscle increases with age, advancing age is characterized by an imbalance between an increase in ROS production in the organism and antioxidant defenses as a whole. Finally, we analyze data, present in literature, regarding the beneficial effects of nutrition and physical activity in preventing oxidative damage associated with sarcopenia. This is a preview of subscription content, log in via an institution.
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