How does oxidation work in the body

Oxidative stress can damage cells, proteins, and DNA, which can contribute to aging. The body naturally produces antioxidants to counteract these free radicals. Making certain lifestyle and dietary changes may help reduce oxidative stress. These may include maintaining a healthy body weight, regularly exercising, and eating a balanced, healthful diet rich in fruits and vegetables.

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How does oxidative stress affect the body? Medically reviewed by Stacy Sampson, D. What is it? Free radicals Antioxidants Effects Conditions Risk factors Prevention Summary Oxidative stress is an imbalance of free radicals and antioxidants in the body, which can lead to cell and tissue damage. What is oxidative stress?

Share on Pinterest Many lifestyle factors can contribute to oxidative stress. What are free radicals? What are antioxidants? This seems to be true when children in prepubertal age are exposed to Cd, a well known responsible for an increase in free radicals and oxidative stress, as well as when pregnant women are exposed to the same metallic element. Summarizing, we can affirm that oxidative stress and free radicals are confirmed to be responsible for several pathological conditions affecting different tissues and systems, thus being one of the most important and pervasive harms to human health.

Human body put in place several strategies to counteract the effects of free radicals and oxidative stress, based on enzymatic e. Beside these, there are several exogenous antioxidant molecules of animal or vegetal origin, mainly introduced by diet or by nutritional supplementation.

Here, we will discuss the most relevant nutritional antioxidants and their protective effects for human health. These results were confirmed in vivo, both in mouse and rabbit models of atherosclerosis [ 53 — 55 ]. Macrophage transition to foam cells is one of the earlier and important steps in atherosclerotic lesion formation; CD36 receptor is one of the key players involved, being a scavenger receptor responsible for oxidized-LDL oxLDL uptake from bloodstream [ 56 , 57 ].

Several studies described that vitamin E is able to prevent CD36 mRNA expression induced by cholesterol, thus playing a beneficial role in preventing foam cell formation. A degree of CD36 mRNA reduction was also observed in animals undergoing to vitamin E supplementation under a regimen of high-fat diet [ 66 — 68 ]. Each form of vitamin E seems to have different regulatory effects when it comes to recruit leukocytes to allergic inflammation site, which is however strictly dependent on vascular cell adhesion molecule-1 VCAM-1 [ 78 ].

This phenomenon was observed even in vivo, in a mouse model of allergic lung inflammation [ 80 , 81 ]. Interestingly, a research found a correlation between the prevalence of asthma and the average plasma tocopherol in several countries, based on nutritional consumption of foods and oils rich in tocopherol.

Flavonoid determines i ROS synthesis suppression, inhibition of enzymes, or chelation of trace elements responsible for free radical generation; ii scavenging ROS; and iii improvement of antioxidant defenses [ , ]. Genistein is a soy isoflavone that is probably the most interesting and well-studied flavonoid compound, due to its broad pharmacological activities.

Genistein has been extensively employed as antioxidant in a plethora of studies, showing the potential to scavenge ROS and RNS with a high degree of efficacy. This flavonoid compound is able to improve the antioxidant defenses of a cell, thus prevents apoptotic process through the modulation of several genes and proteins [ ].

In nonhuman primates and rabbits [ , ], dietary-supplemented genistein delayed atherogenesis. An additional study observed an increase in antioxidant protection of LDL and an atheroprotective effect [ ]. In general, soy isoflavones confer protection against lipoprotein oxidation [ — ], as well as against oxidative DNA damage in postmenopausal women [ ], but the point is still debated [ — ].

There are other mechanism that genistein can be used to suppress oxidative stress and related inflammation in the vascular intima layer. Genistein increases the expression of antioxidant enzymes in human prostate cancer cells conferring protection against oxidative DNA damage [ , ].

Briefly, flavonoids are a class of natural compounds extensively present in foods of vegetal origin fruits, oils, seeds, etc. Nonetheless, they need to be managed carefully, and their supplementation into the diet as diet enrichment or as nutraceuticals have to take in account also some potential drawback concerning human health and wellness. Prooxidant agents, beside their well-known detrimental effects on human health, have been investigated and, in some cases, actually used, as therapeutic agents mainly against cancer diseases.

Here, we will briefly discuss two emerging prooxidant compounds showing interesting pharmacological activities, such as ascorbic acid AA and polyphenols, and the most well-known and employed prooxidant in therapy, ionizing radiation.

Ascorbic acid vitamin C is a water-soluble compound classified under the group of natural antioxidants. Ascorbate reacts with ROS, quenching them and promoting the conversion into semihydroascorbate radical, which is a poorly reactive chemical species, thus efficiently reducing the risk of cancer by suppressing free radicals and oxidative stress [ ].

Another study pointed out that AA was able to inhibit Raji cell proliferation, apparently by downregulating the set of genes needed for S-phase progression in actively proliferating cells [ ]. In an in vivo study, guinea pigs supplemented with AA at various doses showed a complete regression of fibrosarcoma and liposarcoma tumors [ ]. In general, there have been several studies assessing the antiblastic activities of AA, mostly in vitro on different cell lines [ — ].

Despite these somehow surprising but still very interesting results, there is the urge of conducting more researches, both in vitro and in vivo, to definitely assess the mode of action and efficacy of AA as prooxidative anticancer agent.

Under conditions like high concentrations, high pH, and the presence of redox-active metals, phenolic compounds can acquire a prooxidant behavior [ , ], mainly based on the generation of an aroxyl radical or a labile complex with a metal cation exerting redox activity. Polyphenols, like caffeic acid, ferulic acid, and apigenin, can exert a prooxidant effect through the increased intracellular production of ROS by NOX [ , ].

Polyphenols can as well induce oxidative stress via transition metals, promoting the generation of hydroxyl radicals through Fenton and Fenton-like reactions; it is important to note that transition metal ions are more represented into cancer than into normal cells [ ]. Prooxidant polyphenols seem to exert their cytotoxic activity by inducing apoptosis and cell cycle arrest via several pathways. Anthocyanins, pigments present in red wine and berry Aronia melanocarpa , Rosaceae, Vaccinium myrtillus , and Ericaceae fruits, cause apoptosis in cancer cells by increasing intracellular ROS formation [ — ].

Esculetin, a coumarin derivative present in plants such as chicory Cichorium intybus and Asteraceae , showed both in vivo and in vitro antiproliferative activity against hepatocellular carcinoma. Human hepatocellular carcinoma SMMC cells incubated with esculetin undergo to mitochondrial membrane potential collapse, with Bcl-2, caspase, and caspasemediated apoptosis [ ]. In addition, esculetin also exerted a cytotoxic effect on HeLa cells inducing redox-dependent apoptosis, even in this case by causing the disruption of mitochondrial membrane potential, cytochrome C release, and caspase activation [ ].

During the last years, a very large amount of in vitro studies investigated the prooxidative effects of polyphenols against cancer cell proliferation and survival, all of them presenting interesting results that nonetheless need to be confirmed by more in-depth researches [ — ]. Although polyphenols showed the pharmacological potential to inhibit tumorigenesis and arrest cancer cell proliferation in animal models, the role of ROS generation is still poorly understood, mainly because a large majority of the in vivo studies are limited to cancer growth arrest and apoptosis evaluation, and rarely or not at all they go deeper in the mechanistic explanation of a potential prooxidant action in vivo [ , ].

The ability of ionizing radiation to counteract proliferation of cancer cells is well explained [ — ] and widely used in clinical practice. In the last decades, there has been an extensive effort to understand the physical and molecular cellular response that follow the exposure to ionizing radiation. It is well recognized that damage to DNA operated by generation of radicals that indirectly cause DNA double-strand beaks DSBs is the most severe kind of damage induced by this prooxidant physical agent [ , ].

These lesions are promptly repaired, as the results of the rapid activation of DSB damage repair mechanism, most importantly nonhomologous end joining or homologous recombination and the execution of a complex and finely tuned sequelae of those cellular signaling pathways belonging to the DNA damage response DDR [ , ].

In the last 2 decades, several technological advancements, like intensity-modulated radiotherapy IMRT , image-guided radiotherapy IGRT , and stereotactic radiotherapy SRT , were put in place to address the need to reach that level of precision required to take advantage from radiation prooxidant activity avoiding, as much as possible, the side effects in terms of oxidative stress-induced cellular damage on healthy cells and tissues.

Oxidative stress and free radicals are generally known to be detrimental to human health. A large amount of studies demonstrates that in fact free radicals contribute to initiation and progression of several pathologies, ranging from CVD to cancer. If it is true that antioxidants can be very useful in preventing, managing, or treating human pathologies, it is true as well that they are not immune to generating adverse effects. On the other hand, some prooxidant compounds or agents can be as well useful to human health, particularly regarding cancer treatment.

We can reach to the conclusion that oxidative stress, as phenomenon, although being one of the major harms to individuals' wellness and health, it can also be exploited as a treatment tool when and if we will be able to operate a fine tuning of this process inside human organism.

The authors are thankful to all members of the Squadrito laboratory for the technical support. Gabriele Pizzino and Natasha Irrera equally contributed to this paper. National Center for Biotechnology Information , U. Oxid Med Cell Longev. Published online Jul Author information Article notes Copyright and License information Disclaimer. Received May 26; Accepted Jul 5. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

This article has been cited by other articles in PMC. Abstract Oxidative stress is a phenomenon caused by an imbalance between production and accumulation of oxygen reactive species ROS in cells and tissues and the ability of a biological system to detoxify these reactive products. Physiological Activities of Free Radicals When maintained at low or moderate concentrations, free radicals play several beneficial roles for the organism.

Detrimental Effects of Free Radicals on Human Health As stated before, if in excess, free radicals and oxidants give rise to a phenomenon known as oxidative stress; this is a harmful process that can negatively affect several cellular structures, such as membranes, lipids, proteins, lipoproteins, and deoxyribonucleic acid DNA [ 16 — 21 ].

Cardiovascular Disease and Oxidative Stress Cardiovascular diseases CVDs are clinical entities with a multifactorial etiology, generally associated with a very large amount of risk factors, the most broadly recognized of which are hypercholesterolaemia, hypertension, smoking habit, diabetes, unbalanced diet, stress, and sedentary life [ 11 , 30 , 31 ].

Neurological Disease and Oxidative Stress Oxidative stress has been linked to several neurological diseases i. Respiratory Disease and Oxidative Stress Several researches pointed out that lung diseases such as asthma and chronic obstructive pulmonary disease COPD , determined by systemic and local chronic inflammation, are linked to oxidative stress [ 36 — 39 ].

Rheumatoid Arthritis and Oxidative Stress Rheumatoid arthritis is a chronic inflammatory disorder affecting the joints and surrounding tissues, characterized by macrophages and activated T cell infiltration [ 15 , 40 , 41 ]. Kidney Diseases and Oxidative Stress Oxidative stress is involved in a plethora of diseases affecting renal apparatus such as glomerulo- and tubule-interstitial nephritis, renal failure, proteinuria, and uremia [ 16 , 42 ].

Sexual Maturation and Oxidative Stress Several authors pointed out that oxidative stress could be responsible for a delayed sexual maturation and puberty onset [ 46 , 47 ]. Exogenous Antioxidants and Human Health Human body put in place several strategies to counteract the effects of free radicals and oxidative stress, based on enzymatic e. Prooxidant Agents in Therapy Prooxidant agents, beside their well-known detrimental effects on human health, have been investigated and, in some cases, actually used, as therapeutic agents mainly against cancer diseases.

Ascorbic Acid Ascorbic acid vitamin C is a water-soluble compound classified under the group of natural antioxidants.

Polyphenols Under conditions like high concentrations, high pH, and the presence of redox-active metals, phenolic compounds can acquire a prooxidant behavior [ , ], mainly based on the generation of an aroxyl radical or a labile complex with a metal cation exerting redox activity. Radiation Therapy The ability of ionizing radiation to counteract proliferation of cancer cells is well explained [ — ] and widely used in clinical practice.

Conclusions Oxidative stress and free radicals are generally known to be detrimental to human health. Acknowledgments The authors are thankful to all members of the Squadrito laboratory for the technical support. Conflicts of Interest The authors state no conflict of interest. References 1. Sato H. Differential cellular localization of antioxidant enzymes in the trigeminal ganglion.

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Metals, toxicity and oxidative stress. Current Medicinal Chemistry. Parthasarathy S. Oxidants and antioxidants in atherogenesis: an appraisal. Journal of Lipid Research. Frei B. Reactive Oxygen Species and Antioxidant Vitamins. Nishida N. Reactive oxygen species induce epigenetic instability through the formation of 8-hydroxydeoxyguanosine in human hepatocarcinogenesis.

Digestive Diseases. Yasui M. Tracing the fates of site-specifically introduced DNA adducts in the human genome. DNA Repair Amst ; 15 — Valavanidis A. Pulmonary oxidative stress, inflammation and cancer: respirable particulate matter, fibrous dusts and ozone as major causes of lung carcinogenesis through reactive oxygen species mechanisms. It is thought that DA acts as an endogenous neurotoxin, contributing to the pathology of neurodegenerative disorders and ischemia-induced damage in the striatum [ 24 , , ].

Photosensitization reactions involve the oxidation of organic compounds by atmospheric oxygen upon exposure to visible light. The photoexcitated state, most often the triplet state of the sensitizer, is the key photoreactive intermediate and exerts photodamage through direct reaction with substrate molecules type I photosensitization or activation of molecular oxygen by energy transfer reactions type II photosensitization [ ].

The formation of O 2 - as a precursor of H 2 O 2 occurs via electron transfer via production of a sensitizer radical cation, or after an intermediate reduction of the sensitizer with a substrate followed by the single electron reduction of O 2 [ 38 , 99 ].

The most studied producers of O 2. Electrons leaking from nuclear membrane cytochrome oxidases and electron transport systems may give rise to ROS [ 75 ]. In addition to intracellular membrane-associated oxidases, aldehyde oxidase, dihydroorotate dehydrogenase, flavoprotein dehydrogenase and tryptofan dioxygenase can all generate ROS during catalytic cycling.

Auto-oxidation of small molecules such as epinephrine, flavins, and hydroquinones can also be an important source of intracellular ROS production [ 57 ]. During plant photosynthesis and in analogous reactions of the respiratory chain, triplet oxygen is reduced to water reaction 3. As a result of one-, two- and three- electron reduction, toxic forms of oxygen, free radicals and covalent compounds are produced as side products and oxidize additional biomolecules [ ].

If not, 1 O 2 can lead to gene upregulation, involved in the molecular defence responses against photooxidative stress [ ]. The hydrogen donor for the reduction of PUFAs may well be ascorbic acid, forming H 2 O 2 and a radical of ascorbic acid.

Enzymatic dismutation to H 2 O 2 is the most effective quenching mechanism reactions 7, 8. H 2 O 2 is moderately reactive and has a relatively long half-life 1 ms [ 19 ].

It is broken down partially enzymatically by catalase or glutathione peroxidase to water or in case of substrate peroxides to corresponding alcohols and water. In cases where the speed of its decomposition is not sufficient, it may lead to its one-electron reduction reaction However, a recent discovery, that the upper limit of free pools of Cu is far less than a single atom per cell casts serious doubt on the role of Cu in Fenton-like generation of free radicals [ ].

It predominantly attacks the unsaturated fatty acids of membranes. Resulting hydroperoxides R-O-OH are released by phospholipase A 2 , which makes them available substrates for peroxidases. This is considered to be the most damaging process known to occur in living organisms [ 62 ].

It includes a number of reactions leading to the development of oxidized lipids and fatty acids that give rise to free radicals.

Oxidation products of lipids, particularly 2 E hydroxyalkenals and aldehydes such as malondialdehyde, as well as alkanes, lipid epoxides and alcohols, react with proteins and nucleic acids. The overall effects of lipid oxidation are a decrease in membrane fluidity, an increase in the leakiness of the membrane to substances that do not normally cross it except through specific channels and damage to membrane proteins, and inactivation of receptors, enzymes, and ion channels.

The most common oxidation of fatty acids is by 3 O 2 from the air. Oxidation of unsaturated fatty acids only occurs in three stages at normal temperatures. The energy required to split bonds can come from ultraviolet radiation, radioactivity, and also visible light. In the latter case, it is a two-electron oxidation of 1 O 2. A reaction also exists to break any binding with other free radicals or transition metals. The initiation rate of oxidation for the production of R-O-OH is slow induction period leading to a gradual accumulation of R-O-OH, followed by the creation of other radicals.

As long as there is enough oxygen, the reaction takes place spontaneously, sharply rising to reach the maximum speed of reaction, in which reactive groups are diminished.

The rate of this reaction then slows and starts to be overtaken by the degradation of R-O-OH. When the concentration of free radicals is high, it is likely that these will react together to form a nonradical product, which terminates the chain reaction.

This reaction becomes easier as the number of double bonds increases. However, if the number of double bonds is unchanged, the double bond moves one carbon closer to the carboxyl or methylene end of the chain. By moving the double bonds, a double bond in the cis configuration is changed to more stable trans configuration.

R-O-OH of fatty acids and their radicals may react in three ways. In the first case, there is no change in the number of carbon atoms in the molecule.

R-O-OH species from polyunsaturated fatty acids PUFAs containing three or more double bonds in a molecule are unstable, and they tend to pass in 1,4 cyclization to the six-member peroxides derived from 1,2-dioxanes, which are also unstable compounds and decompose to low molecular active products.

R-O-OH molecules by 1,3 cyclisation pass to five-member peroxides, 1,2-dioxolanes and endoperoxides. The main malondialdehyde precursors emerge from 1,2 dioxolane-type peroxohydroperoxides. R-O-OH is oxidized by the nonradical mechanism and the resulting epoxide is immediately hydrolyzed to dihydroxyderivatives.

In the second case, the molecule breaks and gives volatile and sensory active substances with less carbon atoms. From this, saturated and unsaturated aldehydes, saturated and unsaturated hydrocarbons, and oxo acids are formed.

The most reactive compounds formed are aldehydes, which are further oxidized and react with the proteins. Malondialdehyde is an important product of this oxidation [ ]. The third mechanism is oxypolymerization, in which the number of carbons in the molecule is increased due to the reduction of two radicals.

Excitation of the common 3 O 2 leads to a reactive 1 O 2 which may react with the double bond of unsaturated lipids and other unsaturated compounds.

It reacts with the listed compounds because they are rich in electrons and are therefore able to fill its free molecular orbital [ ]. The rate of reaction between common unsaturated acids and 1 O 2 is at least fold higher in comparison to the reaction with triplet oxygen.

Unstable cyclic peroxide compounds moloxides with four or six-member rings are formed by adduction across double bonds. Intermediate products of the reaction decompose rapidly and give rise to respective hydroperoxides. By the reaction with an atom in methylene groups on the carboxyl end of fatty acids, R-O-OH arises in a similar process to peroxide oxidation by 3 O 2. However, the mechanism of primary production of hydroperoxides differs from the mechanisms of 3 O 2 oxidation, therefore producing a different ratio of constitutional isomers.

This type of oxidation is catalyzed by compounds of transition metals, especially Fe and Cu, which are present in tissues that are reduced by accepting an electron. They are involved directly or indirectly in initiation, propagation and termination reactions of radicals [ ].

Subsequently, the oxidation reaction is catalyzed by the ROS produced. These emerging radicals increase the reaction rate by increasing the propagation phase rate, as the metal-catalyzed R-O-OH disintegration is faster than the emergence of new radicals. Metals bound in complexes might or might not be effective depending on the environment.

The rate constant for this reaction when ferrous ions are involved, has been given as 1. The redox potentials of the metals Mn and Co are low and are therefore incapable of catalyzing the breakdown of R-O-OH in aqueous systems. In this mechanism, peroxidase donates two electrons to H 2 O 2 resulting in cleavage of H 2 O 2 and formation of a redox intermediate of enzyme I. This intermediate consists of an oxoferryl protein cation radical, in which one of the oxidation equivalents exists as the ferryl ion and the other as a porphyrin-centred cation radical reaction The enzyme intermediate reacts with reductants R-H to generate substrate free radicals and another redox intermediate II , in which oxoferryl species remain intact but the cation radical is reduced.

A one-electron reduction of II by a second molecule of reductant regenerates the ferric enzyme and forms a second equivalent of R reaction Another redox intermediate III is formed in the course of peroxidase catalytic cycle reaction Some metal ions with a fixed oxidation number can affect the rate of peroxidation, e. Exposure to heavy metals can change the composition of the reaction products.

High concentrations of free radicals may outweigh termination reactions, where the metals inhibit the oxidation. Inhibition of oxidation may occur with higher concentrations of metal ions. It is supposed that Fe and Cu ions oxidize and reduce hydrocarbon free radicals to their corresponding anions reaction 38 and cations reaction 39 together with the emergence of free radical complexes reaction Other complexes are formed with Co reactions All of them break the radical chain reaction.

Free peroxyl radicals react with proteins and produce protein radicals, which then react with other free protein radicals to form dimers, or with free lipid radicals to form copolymers. A hydroxyl acid is obtained from an alkoxyl radical, and hydroperoxide from a peroxyl radical.

Recombination of protein radicals leads subsequently to protein oligomeres. O 2 oxidation of thiol groups —SH leads to disulfide formation —S-S- and vice versa.

Under normal conditions, dehydrogenases have the same effect in organisms, such as the oxidation of Cys to cysteine, for example. The first stage of oxidation is the emergence of alkylthiolate RS - in the presence of the hydroxyl anion HO - reaction The second stage is the reactions with thiols and their emerging radicals reaction 46, In response to the reaction of protein thiols PrS with R-O-OH, atoms of sulfur are simultaneously oxidized frequently those in Cys , forming corresponding monoxides thiosulfinates and, where appropriate, further oxidized products containing 2 sulfoxide groups disulfoxide , sulfone moiety dioxide, thiosulfonate , sulfoxide and sulfone miety sulfoxido sulfone, trioxides , and 2 sulfone groups disulfonates, tetraoxides [ ].

Reactions with hydro and hydrogen peroxides convert thiol proteins also into sulfenic acids RSOH , which can be further oxidized to higher oxidation states such as sulfinic RSO 2 H and sulfonic RSO 3 H acids [ 85 , ]. Proteins, lipids, and DNA make up a large part of your body, so that damage can lead to a vast number of diseases over time.

These include:. Everyone produces some free radicals naturally in their body through processes like exercise or inflammation. However, there are things you can do to minimize the effects of oxidative stress on your body. The main thing you can do is to increase your levels of antioxidants and decrease your formation of free radicals. Eating five servings per day of a variety of fruits and vegetables is the best way to provide your body what it needs to produce antioxidants.

Examples of fruits and vegetables include:. Other healthy lifestyle choices can also prevent or reduce oxidative stress. Here are some lifestyle choices that will help:. Oxidative stress can cause damage to many of your tissues, which can lead to a number of diseases over time.

Antioxidants are incredibly important, but most people don't really understand what they are. This article explains it all in human terms. Exercising regularly has many benefits for your body and brain.