Oxidative stress treatment -
Chemically, oxidative stress is associated with increased production of oxidizing species or a significant decrease in the effectiveness of antioxidant defenses, such as glutathione. However, more severe oxidative stress can cause cell death, and even moderate oxidation can trigger apoptosis , while more intense stresses may cause necrosis.
Production of reactive oxygen species is a particularly destructive aspect of oxidative stress. Such species include free radicals and peroxides. Some of the less reactive of these species such as superoxide can be converted by oxidoreduction reactions with transition metals or other redox cycling compounds including quinones into more aggressive radical species that can cause extensive cellular damage.
Biological effects of single-base damage by radiation or oxidation, such as 8-oxoguanine and thymine glycol , have been extensively studied. Recently the focus has shifted to some of the more complex lesions. Tandem DNA lesions are formed at substantial frequency by ionizing radiation and metal- catalyzed H 2 O 2 reactions.
Under anoxic conditions , the predominant double-base lesion is a species in which C8 of guanine is linked to the 5-methyl group of an adjacent 3'-thymine G[8,5- Me]T. Normal cellular defense mechanisms destroy most of these.
Repair of oxidative damages to DNA is frequent and ongoing, largely keeping up with newly induced damages. In rat urine, about 74, oxidative DNA adducts per cell are excreted daily.
There are about 24, oxidative DNA adducts per cell in young rats and 66, adducts per cell in old rats. However, under the severe levels of oxidative stress that cause necrosis, the damage causes ATP depletion, preventing controlled apoptotic death and causing the cell to simply fall apart.
Polyunsaturated fatty acids , particularly arachidonic acid and linoleic acid , are primary targets for free radical and singlet oxygen oxidations. For example, in tissues and cells, the free radical oxidation of linoleic acid produces racemic mixtures of hydroxy-9 Z ,11 E -octadecadienoic acid, hydroxy-9 E ,11 E -octadecadienoic acid, 9-hydroxy E , E -octadecadienoic acid 9-EE-HODE , and hydroxy-9 Z , Z -octadecadienoic acid as well as 4-Hydroxynonenal while singlet oxygen attacks linoleic acid to produce presumed but not yet proven to be racemic mixtures of hydroxy-9 Z ,11 E -octadecadienoic acid, 9-hydroxy E , Z -octadecadienoic acid, hydroxy-8 E ,12 Z -octadecadienoic acid, and hydroxy-9 Z E -octadecadienoic see Hydroxyoctadecadienoic acid and 9-Hydroxyoctadecadienoic acid.
For example, the presence of racemic 9-HODE and 9-EE-HODE mixtures reflects free radical oxidation of linoleic acid whereas the presence of racemic hydroxy-8 E ,12 Z -octadecadienoic acid and hydroxy-9 Z E -octadecadienoic acid reflects singlet oxygen attack on linoleic acid.
Table adapted from. One source of reactive oxygen under normal conditions in humans is the leakage of activated oxygen from mitochondria during oxidative phosphorylation.
coli mutants that lack an active electron transport chain produce as much hydrogen peroxide as wild-type cells, indicating that other enzymes contribute the bulk of oxidants in these organisms.
Other enzymes capable of producing superoxide are xanthine oxidase , NADPH oxidases and cytochromes P Hydrogen peroxide is produced by a wide variety of enzymes including several oxidases.
Reactive oxygen species play important roles in cell signalling, a process termed redox signaling. Thus, to maintain proper cellular homeostasis , a balance must be struck between reactive oxygen production and consumption. The best studied cellular antioxidants are the enzymes superoxide dismutase SOD , catalase , and glutathione peroxidase.
Less well studied but probably just as important enzymatic antioxidants are the peroxiredoxins and the recently discovered sulfiredoxin. Other enzymes that have antioxidant properties though this is not their primary role include paraoxonase, glutathione-S transferases, and aldehyde dehydrogenases.
The amino acid methionine is prone to oxidation, but oxidized methionine can be reversible. Oxidative stress is suspected to be important in neurodegenerative diseases including Lou Gehrig's disease aka MND or ALS , Parkinson's disease , Alzheimer's disease , Huntington's disease , depression , and multiple sclerosis.
Oxidative stress is thought to be linked to certain cardiovascular disease , since oxidation of LDL in the vascular endothelium is a precursor to plaque formation. Oxidative stress also plays a role in the ischemic cascade due to oxygen reperfusion injury following hypoxia.
This cascade includes both strokes and heart attacks. In hematological cancers, such as leukemia, the impact of oxidative stress can be bilateral. Reactive oxygen species can disrupt the function of immune cells, promoting immune evasion of leukemic cells.
On the other hand, high levels of oxidative stress can also be selectively toxic to cancer cells. Oxidative stress is likely to be involved in age-related development of cancer. The reactive species produced in oxidative stress can cause direct damage to the DNA and are therefore mutagenic , and it may also suppress apoptosis and promote proliferation, invasiveness and metastasis.
Oxidative stress can cause DNA damage in neurons. The use of antioxidants to prevent some diseases is controversial. The American Heart Association therefore recommends the consumption of food rich in antioxidant vitamins and other nutrients, but does not recommend the use of vitamin E supplements to prevent cardiovascular disease.
AstraZeneca 's radical scavenging nitrone drug NXY shows some efficacy in the treatment of stroke. Oxidative stress as formulated in Denham Harman 's free-radical theory of aging is also thought to contribute to the aging process.
While there is good evidence to support this idea in model organisms such as Drosophila melanogaster and Caenorhabditis elegans , [67] [68] recent evidence from Michael Ristow 's laboratory suggests that oxidative stress may also promote life expectancy of Caenorhabditis elegans by inducing a secondary response to initially increased levels of reactive oxygen species.
The USDA removed the table showing the Oxygen Radical Absorbance Capacity ORAC of Selected Foods Release 2 table due to the lack of evidence that the antioxidant level present in a food translated into a related antioxidant effect in the body.
Metals such as iron , copper , chromium , vanadium , and cobalt are capable of redox cycling in which a single electron may be accepted or donated by the metal.
This action catalyzes production of reactive radicals and reactive oxygen species. These metals are thought to induce Fenton reactions and the Haber-Weiss reaction, in which hydroxyl radical is generated from hydrogen peroxide. For example, meta- tyrosine and ortho- tyrosine form by hydroxylation of phenylalanine.
Other reactions include lipid peroxidation and oxidation of nucleobases. Metal-catalyzed oxidations also lead to irreversible modification of arginine, lysine, proline, and threonine. Excessive oxidative-damage leads to protein degradation or aggregation.
The reaction of transition metals with proteins oxidated by reactive oxygen or nitrogen species can yield reactive products that accumulate and contribute to aging and disease.
For example, in Alzheimer's patients, peroxidized lipids and proteins accumulate in lysosomes of the brain cells. Certain organic compounds in addition to metal redox catalysts can also produce reactive oxygen species.
One of the most important classes of these is the quinones. Quinones can redox cycle with their conjugate semiquinones and hydroquinones , in some cases catalyzing the production of superoxide from dioxygen or hydrogen peroxide from superoxide.
The immune system uses the lethal effects of oxidants by making the production of oxidizing species a central part of its mechanism of killing pathogens; with activated phagocytes producing both reactive oxygen and nitrogen species.
Sperm DNA fragmentation appears to be an important factor in the aetiology of male infertility , since men with high DNA fragmentation levels have significantly lower odds of conceiving. In a rat model of premature aging, oxidative stress induced DNA damage in the neocortex and hippocampus was substantially higher than in normally aging control rats.
However, it was recently shown that the fluoroquinolone antibiotic Enoxacin can diminish aging signals and promote lifespan extension in nematodes C. elegans by inducing oxidative stress.
The great oxygenation event began with the biologically induced appearance of oxygen in the Earth's atmosphere about 2.
The rise of oxygen levels due to cyanobacterial photosynthesis in ancient microenvironments was probably highly toxic to the surrounding biota. Under these conditions, the selective pressure of oxidative stress is thought to have driven the evolutionary transformation of an archaeal lineage into the first eukaryotes.
Selective pressure for efficient repair of oxidative DNA damages may have promoted the evolution of eukaryotic sex involving such features as cell- cell fusions , cytoskeleton -mediated chromosome movements and emergence of the nuclear membrane. It has been proposed that oxidative stress may play a major role in determining cardiac complications in COVID Free radicals arise as byproducts of this metabolic process.
External substances, such as cigarette smoke, pesticides, and ozone, can also cause the formation of free radicals in the body. Antioxidants are substances that neutralize or remove free radicals by donating an electron. The neutralizing effect of antioxidants helps protect the body from oxidative stress.
Examples of antioxidants include vitamins A, C, and E. Like free radicals, antioxidants come from several different sources. Cells naturally produce antioxidants such as glutathione. Foods such as fruits and vegetables provide many essential antioxidants in the form of vitamins and minerals that the body cannot create on its own.
The effects of oxidative stress vary and are not always harmful. For example, oxidative stress that results from physical activity may have beneficial, regulatory effects on the body. Exercise increases free radical formation, which can cause temporary oxidative stress in the muscles.
However, the free radicals formed during physical activity regulate tissue growth and stimulate the production of antioxidants. Mild oxidative stress may also protect the body from infection and diseases. In a study , scientists found that oxidative stress limited the spread of melanoma cancer cells in mice.
This can contribute to aging and may play an important role in the development of a range of conditions. Immune cells called macrophages produce free radicals while fighting off invading germs. These free radicals can damage healthy cells, leading to inflammation. Under normal circumstances, inflammation goes away after the immune system eliminates the infection or repairs the damaged tissue.
However, oxidative stress can also trigger the inflammatory response, which, in turn, produces more free radicals that can lead to further oxidative stress, creating a cycle. Chronic inflammation due to oxidative stress may lead to several conditions, including diabetes, cardiovascular disease, and arthritis.
The brain is particularly vulnerable to oxidative stress because brain cells require a substantial amount of oxygen. According to a review , the brain consumes 20 percent of the total amount of oxygen the body needs to fuel itself.
Brain cells use oxygen to perform intense metabolic activities that generate free radicals. These free radicals help support brain cell growth, neuroplasticity, and cognitive functioning. Oxidative stress also alters essential proteins, such as amyloid-beta peptides.
According to one systematic review , oxidative stress may modify these peptides in way that contributes to the accumulation of amyloid plaques in the brain. It is important to remember that the body requires both free radicals and antioxidants.
Having too many or too few of either may lead to health problems. Maintaining a healthy body weight may help reduce oxidative stress. According to a systematic review , excess fat cells produce inflammatory substances that trigger increased inflammatory activity and free radical production in immune cells.
The body produces free radicals during normal metabolic processes. Oxidative stress can damage cells, proteins, and DNA, which can contribute to aging. The body naturally produces antioxidants to counteract these free radicals.
In the case of antioxidants, studies show that more does not necessarily mean better. Consuming superfoods does not compensate for other unhealthy eating habits or an unbalanced lifestyle. Free radicals, as well as antioxidants, can have beneficial effects on the body.
Therefore, we are talking about a balance and not a negative role attributed to free radicals and a positive one to antioxidants. Degradation of nucleic acids, proteins, lipids or other cellular components are among the effects that an excessive concentration of free radicals can generate.
Risk factors leading to free radicals include air pollution, ionizing radiation, prolonged exercise, infections, excessive consumption of polyunsaturated fatty acids Poprac et al.
On the other hand, antioxidants are considered to be the solution to these problems — substances that neutralize free radicals. In some situations, some substances act as antioxidants, in other situations they become prooxidants, depending on the chemical composition of the environment in which they are.
There are many types of antioxidants, and the role in the body and the mechanisms by which they act are different. One misconception is that one antioxidant can be replaced with another, having the same effect.
In fact, each has its own unique biological properties Chen X. There is also a significant difference between taking antioxidants from food and administering an isolated substance as a supplement. Many substances that demonstrate beneficial effects in the laboratory do not work when introduced into the human body.
Many antioxidants do not have good bioavailability. The concentration of antioxidants such as polyphenols is sometimes so low in the blood that no significant effect is observed Fernández-García et al. Fruits and vegetables contain bioactive substances that in many cases do not work as antioxidants if we consider them outside of the body.
But they work as antioxidants when they are in the body, because they activate their own antioxidant mechanisms. These bioactive substances are the secret behind vegetable consumption Kurutas, Antioxidant supplements may have different health benefits.
On the one hand, it is possible that other substances present in food are responsible for the positive effects on health, not necessarily a certain type of antioxidant, but the synergistic effect of several substances.
On the other hand, the chemical structure of antioxidants in food is often different from that identified in supplements. An example is vitamin E. There are eight variants of vitamin E in the foods we eat, while the supplements used in most studies contain only one form Firuzi et al.
Studies also frequently include healthy people, for whom oxidative stress on the body is not significant to determine a risk of disease. Antioxidants can benefit certain categories of patients in whom there is a real, documented imbalance, but it may not bring anything extra for a person who gets a sufficient amount of nutrients from their diet.
Observational studies analyze the trends, or habits of certain large population groups. In many, all the risk factors that could influence the course of the study can be controlled, and demonstrating a cause-effect relationship is difficult.
We also cannot rely on small studies, carried out over a short period of time and using very concentrated substances extracted from different plant or animal products, to say that we have a superfood. Nutrition is a complex science, and at the moment we can only rely on the evidence accumulated so far.
A food rich in antioxidants will not compensate for an unhealthy lifestyle. Oxidative stress can be reduced by approaching a balanced lifestyle. Nutrition plays a critical role, and the best treatment against oxidative stress is antioxidants.
Oxidative stress plays an important role in the pathogenesis of potentially severe conditions. In the long term, increasing the level of prooxidant factors can cause structural defects in mitochondrial DNA and alterations in enzymatic functionality or cellular structures, with the appearance of functional, structural abnormalities or aberrations in gene expression.
It has also been shown that in addition to metabolic products, other external agents can have a prooxidant effect, which has led to the conclusion that lifestyle and diet can play an important role in controlling oxidative stress.
Plant-derived bioactive molecules have gained pivotal attention in recent years, given their therapeutic relevance in both disease prevention and treatment, whether using the whole plants, plant extracts or even the isolated constituents with full phytochemical profiles.
The daily intake of a wide variety of phytochemicals has shown to be chemopreventive. It might hold promise for add-on treatment for several diseases, including cancer, diabetes, cardiovascular disease and neurodegenerative disorders.
Larger randomized trials are needed to obtain clear scientific evidence on the benefits or risks of antioxidant supplementation during cancer treatment. Antioxidants are also prone to oxidation, and therefore their use as foods or supplements should be carefully considered because oxidation and reduction reactions do not happen in isolation.
The intake of high doses of antioxidants has been increasingly highlighted since there is increasing evidence of some detrimental effects. The study of their chemical components as future prophylactic and therapeutic agents would be of particular interest, as they are more effective and safer than those widely available.
In conclusion, oxidative stress is an important pathogenetic link for humans and studies in this field may be important elements in the future, to better understand and manage various diseases.
JS-R and MS-R contributed to the conceptualization. NA, PZ, EV, and LD contributed to the validation investigation. EP, JR, PT, EA, IP, YE, and MB contributed to the resources. AP, MN, and AD: data curation. MS-R, AD, LP, MI, NM, MM, WS, DC, WC, and JS-R contributed to the review and editing. All authors contributed to the writing of the manuscript.
All authors read and approved the final manuscript and contributed equally to the manuscript. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. NM would like to thank the Portuguese Foundation for Science and Technology FCT—Portugal for the Strategic project ref.
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