Antioxidants and free radicals
October 1, 2026
We have received the following article from Klaus Sall regarding fundamental concepts and theories in the biochemistry of free radicals and antioxidants.
The article is highly detailed and likely appeals primarily to specialists; therefore, the Vital Council has taken the liberty of starting with a greatly condensed “primer” version of Klaus Sall’s article for interested readers whose familiarity with biochemistry may be somewhat limited.
Immediately following this is Klaus Sall’s in-depth article, complete with figures, tables, and references.
Read it to gain further insight into the specific points raised and to view a series of explanatory figures that provide a deeper understanding of this important subject—which forms the basis for all life on this planet.
Take care of yourself and others.
Claus Hancke
Specialist in general medicine
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Antioxidants and free radicals (abbreviated)
On oxidative stress in cells and organs and the effects of antioxidants such as vitamin C and vitamin E, as well as iron, copper, and heavy metals.
By Klaus Sall, biologist (abridged by the Vitality Council)
Free radicals and oxidative stress
Electrons “prefer” to exist in pairs. An atom or molecule with an unpaired electron is called a free radical and is often highly reactive. Free radicals can acquire an electron or an entire hydrogen atom from other molecules, thereby transforming them into new radicals. This can trigger chain reactions that damage cellular molecules.
Many of the body’s free radicals are oxygen-based and are referred to as Reactive Oxygen Species (ROS). ROS are not solely harmful; in small, controlled amounts, they play a vital role in cell signaling and are used by the immune system, among other things, to combat microorganisms.
The problem arises when ROS production exceeds the cells’ ability to neutralize them and repair the damage they cause. This imbalance is known as oxidative stress. Oxidative stress is associated with aging and a range of disease processes, including cardiovascular, neurological, and metabolic disorders, as well as cancer.
The body’s primary defense against oxidative stress is its antioxidant system. An antioxidant can be defined as a molecule that delays, prevents, or eliminates oxidative damage. This defense mechanism comprises several layers: preventing the formation of free radicals, enzymes that neutralize them, antioxidants that interrupt chain reactions, and the repair or removal of damaged molecules.
Damage to membranes, proteins, and DNA
Free radicals can damage three of the cell’s most important structures: membranes, proteins, and DNA/RNA. Oxidative damage is also closely linked to chronic low-grade inflammation. The combination of ROS and inflammation can contribute to the gradual deterioration of cells, tissues, and organs with age—a phenomenon often referred to as “inflamm-aging.”
Cell membranes are particularly vulnerable because they contain unsaturated fatty acids. A free radical can remove a hydrogen atom from a fatty acid, thereby turning the fatty acid itself into a radical. This can trigger a chain reaction—lipid peroxidation—in which the damage spreads across the membrane. Vitamin E can halt this chain reaction, while Vitamin C can subsequently help regenerate Vitamin E into its active form. Antioxidants thus function as a collaborative network.
Proteins can also be attacked. Alterations to individual amino acids can cause enzymes to lose their function or misfold. Sulfur-containing amino acids—specifically cysteine and methionine—are particularly susceptible to oxidation.
In DNA and RNA, free radicals can oxidize the bases and cause strand breaks. If DNA damage is not repaired correctly, it can be passed on as mutations during cell division. Mitochondrial DNA is especially vulnerable, partly because it is located close to a major source of ROS.
The body’s own antioxidant system is supplemented by antioxidants from the diet. Among the most important are vitamins C and E, but a range of plant compounds—such as flavonoids, tannins, carotenoids, and Q10—can also influence the redox balance.
Mitochondria and the body’s antioxidant defense
When cells convert nutrients into energy, a significant part of the process takes place in the mitochondrial electron transport chain. Here, electrons are transferred to oxygen in controlled steps, while the energy released is used to generate ATP.
However, a small fraction of the electrons can “leak” and react with oxygen, leading to the formation of substances such as superoxide (O₂•⁻) and hydrogen peroxide (H₂O₂). Although hydrogen peroxide is not a free radical itself, under certain conditions it can be converted into the highly reactive hydroxyl radical (OH•).
The cells’ primary enzymatic antioxidant defenses include superoxide dismutase (SOD), catalase, and glutathione peroxidases (GPx). These enzymes work in concert: SOD converts superoxide into hydrogen peroxide, after which catalase and the glutathione system can convert the hydrogen peroxide into harmless products.
The hydroxyl radical reacts so rapidly that cells lack an enzyme capable of directly “scavenging” it. Consequently, the primary strategy is to prevent its formation.
Iron and copper play a crucial dual role in this context. Both metals are essential to the organism when properly bound within proteins and enzymes. Conversely, free iron and copper can react with hydrogen peroxide to generate hydroxyl radicals through so-called Fenton reactions. Therefore, the body normally keeps iron and copper tightly bound to proteins such as transferrin and ferritin.
Dietary antioxidants
The body’s own antioxidant system is supplemented by antioxidants from the diet. Among the most important are vitamins C and E, though various plant compounds—such as flavonoids, tannins, and carotenoids—can also influence redox balance.
Vitamin C is water-soluble and is found primarily in blood plasma, the cytosol, and the extracellular fluid. It can donate electrons to radicals, thereby terminating radical reactions. Furthermore, vitamin C can help regenerate vitamin E.
Vitamin E is fat-soluble and is found in locations such as cell membranes and lipoproteins. Here, it acts as a crucial “chain-breaking” agent capable of halting lipid peroxidation, thereby limiting damage to membrane lipids.
What matters, therefore, is not any single antioxidant, but rather a network of antioxidants that operate in different parts of the cell and support one another.
Heavy metals and oxidative stress
Heavy metals such as mercury, cadmium, and arsenic can increase oxidative stress in several ways. They can disrupt mitochondrial electron transport, thereby increasing the formation of ROS. At the same time, they can impair the cells’ antioxidant defenses.
Mercury and cadmium, for instance, bind strongly to sulfur-containing molecules and can thus affect glutathione and sulfur-containing proteins. Arsenic can likewise affect redox systems and energy metabolism. Aluminum can, among other things, affect how cells handle iron and mercury, thereby indirectly contributing to increased free radical formation.
Balance is crucial
Free radicals (ROS) are not solely harmful. In small, controlled amounts, ROS are essential for normal biological functions, including cell signaling and immune system activity. The problem arises when there are insufficient antioxidants to neutralize ROS.
Oxidative stress is exacerbated by heavy metals or excessive levels of iron and copper; it can damage cell membranes, proteins, DNA, and mitochondria, contributing to inflammation, disease, and accelerated aging.
The key takeaway: Free radicals serve important biological functions but must remain in balance with antioxidants derived from the body and the diet.
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Antioxidants and free radicals (unabbreviated)
On oxidative stress in cells and organs and the effects of antioxidants such as vitamin C and vitamin E, as well as iron, copper, and heavy metals.
By Klaus Sall, Biologist
Odd and even numbers of electrons
Most people are familiar with the idea that ions can trigger chemical reactions because they carry an electric charge—with positive charges attracted to negative ones. However, in biological chemistry, there is another driving force that is at least as important for chemical reactions: free radicals. Electrons prefer to exist in pairs; consequently, an atom or molecule with an unpaired electron becomes eager to acquire—or figuratively “steal”—an electron to achieve an even number of electrons. This explains why free radicals often react rapidly with other molecules, potentially causing them serious damage.
Some of the severe damage free radicals can inflict on cells stems from the fact that many of them do not merely steal an electron but take an entire hydrogen atom from another molecule. When the hydrogen atom is removed along with its electron, the remaining molecule itself becomes a radical. This new radical can then react with other molecules, propagating the damage in a chain reaction.
Free radicals: A free radical can therefore best be defined as:
An atom or molecule with an unpaired electron is a free radical.
To indicate that an atom or molecule is a free radical, a dot (•) is typically placed in the chemical formula, such as H•, OH•, ONOO•, or O2•−. As these examples show, the free radicals in our cells are often associated with oxygen; consequently, they are frequently referred to as “Reactive Oxygen Species,” or ROS.
The beneficial aspect of ROS is that they are essential for normal cell function and division; cells also actively utilize them as a key component of their immune defense to kill bacteria and neutralize viruses.
Oxidative stress: In living organisms, problems associated with ROS arise when ROS production becomes excessive relative to the cell’s system for neutralizing them. High ROS levels place the cell’s repair mechanisms under strain, leading to cellular damage; this imbalance is known as oxidative stress.
Current understanding identifies oxidative stress as a major factor in the aging of the body’s cells and organs, and a direct negative link has been documented between oxidative stress and various adverse processes within cells and organs. For instance, oxidative stress can inhibit the cellular production of nitric oxide (NO)—a process essential for the health of blood vessel walls. There is growing evidence that men—partly due to greater muscle mass—experience higher levels of oxidative stress than women, a factor contributing to women’s longer life expectancy. Oxidative stress increasingly appears to be an underlying cause of many of the diseases that lead to death, such as cardiovascular, neurological, and metabolic disorders, as well as cancer.
Antioxidants are the body’s primary defense against oxidative stress. Cells do not protect themselves with a single universal antioxidant but rather through multiple layers: preventing the formation of free radicals, utilizing enzymes to neutralize free radicals, employing antioxidants to interrupt chain reactions, regenerating antioxidants, and repairing or removing damaged molecules. A useful definition of antioxidants is:
Any molecule that delays, inhibits, or eliminates oxidative damage to a molecule.
Antioxidants can, for example, be molecules capable of donating one or more electrons—or an entire hydrogen atom—without stealing an electron from another molecule. The body’s most important antioxidants are produced within the cells and consist primarily of specialized enzymes such as glutathione, catalase, and superoxide dismutase (SOD). Dietary antioxidants complement and may potentially stimulate the cells’ antioxidant systems, but they cannot replace them.
Part of the cellular antioxidant defense involves preventing the formation of unwanted free radicals within the cell. Although metals such as iron and copper are essential for the functioning of the body and its cells when incorporated into enzymes, these metals promote the production of free radicals when unbound; consequently, cells possess systems that facilitate their binding.
Damage to cell membranes, proteins, and DNA
There is a close link between the damage free radicals can cause to cell membranes, proteins, and DNA/RNA and chronic, low-grade inflammation in the body. The immune system responds to damaged molecules and cells by activating various signaling molecules and immune cells, which can lead to further cellular damage. The connection between free radicals and bodily aging was first proposed in 1956; today, however, the phenomenon is often termed “inflamm-aging.” Since the combination of ROS and inflammation is considered the cause of the gradual deterioration of cells, tissues, and organs that occurs and accumulates with age, perhaps it should be called “oxi-aging” instead.
Damage to the cell’s outer membranes and internal structure
Free radicals can attack the cells’ outer and internal membranes. Cell membranes are composed of a phospholipid bilayer in which each glycerol molecule binds two fatty acids (the long “legs” in the figure on the right) and a phosphate group (blue). Free radicals particularly target the unsaturated fatty acids within the membranes because these contain double bonds. Attached to each of the two carbon atoms sharing a double bond is a single hydrogen atom, which a free radical—such as HO•—can relatively easily abstract. This transforms the fatty acid itself into a fatty acid radical. This can trigger a chain reaction in which an oxygen molecule (O2) binds to the carbon atom, which subsequently abstracts a hydrogen atom from a neighboring fatty acid. This process forms both a fatty acid peroxide and a new fatty acid radical, allowing the chain reaction to continue. The result can be a compromised membrane and a correspondingly impaired cellular function. This chain reaction can persist until, for example, a vitamin E molecule donates a hydrogen atom.
FH + OH• → F• + H₂O (initiation; FH = fatty acid)
F• + O₂ → FOO• (fatty acid peroxyl radical)
FOO• + FH → FOOH + F• (chain reaction)
Vitamin E stops the chain:
FOO• + Tocopherol-OH → FOOH + Tocopherol-O•
Vitamin C regenerates tocopherol:
TocO• + Ascorbic acid-H⁻ → Tocopherol-OH + Ascorbic acid•⁻
The final step illustrates the practical point that antioxidants can function in networks. Vitamin E protects fats, and Vitamin C can help reactivate Vitamin E.
The damaged fatty acids can subsequently be broken down and excreted from the cell as malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE); consequently, the blood concentrations of these two substances can serve as a measure of the body’s ROS load.
Damage to proteins
Proteins are also susceptible to attack by free radicals. Proteins are found throughout the cell in the form of enzymes and the pumps located in all cellular membranes. Free radicals attack specific amino acids within the protein, potentially causing the enzyme to fragment or cross-link, thereby resulting in a loss of function. If the enzyme’s active site, a binding site, or a region stabilizing the enzyme’s folding is affected, a localized change can inactivate the entire protein or promote misfolding and degradation. Sulfur-containing amino acids, such as cysteine and methionine, are particularly vulnerable to attack by free radicals.
DNA and RNA damage – Oxidation, breaks, and mutations
In DNA, HO• can react with both the nucleobases linking the two DNA strands and the sugar-phosphate backbones running along each side of the DNA strand—and similarly with the single-stranded structure of RNA. Consequences can include oxidized bases, single- or double-strand breaks, DNA-protein cross-links, etc. The guanine base is particularly susceptible to oxidation and can serve as a marker for free-radical damage to DNA and RNA.
DNA damage is usually localized, but the biological consequences can be severe if the damage is not repaired or is repaired incorrectly—and especially if the error is propagated when the cell subsequently divides. Mitochondrial DNA and RNA can be particularly vulnerable due to their proximity to ROS production. Furthermore, mitochondrial DNA is not protected by histones and lacks the repair mechanisms that act on the cell’s nuclear DNA.
When the cell’s energy production leaks electrons
When our cells break down sugar and other substances to produce energy, the process occurs primarily through a chain of chemical reactions involving many small steps (the electron transport chain). The vast majority of this energy production takes place in the cell’s mitochondria, where the aim is to capture the chemical energy stored in the bonds holding the sugar molecules’ atoms together. The goal of the electron transport chain is to transfer electrons to oxygen (O₂) in a series of controlled steps, allowing the cell to “harvest” the energy along the way and use it to generate ATP.
However, this controlled electron transport is not entirely error-free. A small fraction of the electrons can be transferred directly to O₂ during the process, resulting in only partial reduction of the oxygen. This can lead to the formation of superoxide (O₂•⁻) and the hydroxyl radical (OH•), which are extremely reactive oxygen species. H₂O₂ is also produced in the mitochondria; while not a reactive oxygen species itself, it is unstable and can, among other things, serve as a precursor for the formation of OH•.
Because ROS can cause severe damage to cells, cells possess multiple layers of enzymes that neutralize ROS; in addition, there are the antioxidants we absorb from food via the gut—primarily vitamins C and E, but also various active plant compounds such as flavonoids, tannins, and carotenoids.
The cells’ antioxidant defense
The three most important enzymes for neutralizing ROS are superoxide dismutase (SOD), catalase, and glutathione peroxidases (GPx), which often work together in a chain.
Superoxide dismutase: One of the ROS species formed in the mitochondria is an ordinary oxygen molecule (O₂) that has acquired an extra electron, thereby becoming superoxide (O₂•⁻). Each of the two oxygen atoms contributes 8 electrons, and when the extra electron is added, the total becomes 8 + 8 + 1 = 17 electrons.
O₂ + e⁻ → O₂•⁻ (= superoxide)
Superoxide (O₂•⁻) is highly reactive, and cells can utilize the enzyme SOD, which catalyzes a reaction converting superoxide into hydrogen peroxide (H₂O₂).
2 O₂•⁻ + 2 H⁺ + SOD → H₂O₂ + O₂ + SOD
Catalase: Hydrogen peroxide (H₂O₂) is produced by SOD, but also when oxygen undergoes incomplete reduction in the mitochondria; consequently, our cells possess enzymes—catalase and glutathione compounds—that constantly work to detoxify hydrogen peroxide in the mitochondria and elsewhere within the cells.
The most specialized enzyme—catalase—facilitates a very simple reaction in which hydrogen peroxide is converted into water and an oxygen molecule:
2 H₂O₂ + catalase → 2 H₂O + O₂ + catalase
As shown, catalase facilitates this reaction without itself undergoing change; the enzyme therefore possesses a very high capacity to neutralize hydrogen peroxide, as it is immediately ready to repeat the reaction.
Unlike the most aggressive free radicals, hydrogen peroxide is relatively stable, and the two enzymes normally maintain the H₂O₂ concentration within narrow limits.
The hydroxyl radical (OH•) reacts extremely rapidly and can attack almost any nearby molecule: DNA, proteins, and especially fatty acids in membranes. It is believed that because OH• reacts so quickly, biological systems have been unable to evolve an enzyme capable of “capturing” it in the same way that, for example, catalase captures its target.
Consequently, the cellular strategy against OH• is indirect: the cell attempts to prevent the formation of OH• altogether. This is where iron and copper play a detrimental role, as they facilitate reactions that generate OH• from H₂O₂. Cells sequester iron by binding it to transferrin and larger molecules like ferritin, while copper is immediately bound to glutathione and various sulfur-containing proteins, or excess copper is exported from the cell in a controlled manner.
Iron and copper can undergo changes in oxidation state (Fe²⁺ to Fe³⁺ and Cu⁺ to Cu²⁺), and if—or when—they are present in a free state within the cell, they can catalyze the breakdown of H₂O₂ to produce OH•:
Fe²⁺ + H₂O₂ → Fe³⁺ + OH• + OH⁻ (Fenton reaction)
Cu⁺ + H₂O₂ → Cu²⁺ + OH• + OH⁻ (Fenton-like reaction)
Unfortunately, superoxide (O₂•⁻) can react with Fe³⁺ and regenerate Fe²⁺ in what is known as a metal-catalyzed Haber–Weiss reaction:
Fe³⁺ + O₂•⁻ → Fe²⁺ + O₂
– after which OH• can again be formed through the interaction of H₂O₂ with free iron.
Here, antioxidants are once again important because they can break the chain of OH• production by donating an electron or a whole hydrogen atom. Similarly, catalase can break down H₂O₂.
Free radicals and antioxidants from diet and the environment
Redox balance is influenced by chemical exposures the body encounters throughout life. The most well-known of these is tobacco smoke, which delivers free radicals—generated during the combustion of tobacco—to lung tissue and subsequently to the rest of the body. However, our food is also a source of both antioxidants and free radicals. Free radicals are produced during bacterial fermentation of food in the gut, but they may already be present before the food reaches our mouths; high-heat cooking, for instance, can transform proteins and fats into free radicals. Conversely, the diet can also provide substances such as vitamins C, E, and K, as well as coenzyme Q10, tannins, beta-carotene, and other carotenoids.
Vitamin C: Water-soluble antioxidant and redox helper
Vitamin C (ascorbate) is primarily found in aqueous environments: blood plasma, the fluid inside cells (cytosol), and the fluid between cells. It can donate electrons to radicals, thereby “terminating” radical reactions. In the process, ascorbate itself becomes a relatively stable intermediate that the body can convert back into its active form. Vitamin C also acts as a helper for other antioxidants; for example, it can regenerate vitamin E after the latter has halted a chain reaction within a membrane.
Vitamin E: Fat-soluble ‘chain-breaker’ in membranes
Vitamin E is a family of tocopherols and tocotrienols, the best-known of which is alpha-tocopherol. Vitamin E is fat-soluble and therefore associates with the outer and inner cell membranes—all composed of various phospholipids—as well as mitochondrial membranes and lipoproteins in the blood.
Vitamin E is particularly important because fatty substances can be oxidized by free radicals, potentially triggering a chain reaction in which one radical generates the next, allowing damage to spread through the membrane.
Heavy metals: Oxidative stress via two main pathways
Heavy metals such as mercury, cadmium, and arsenic can be absorbed through the intestines and lungs and transported via the bloodstream into cells. Although heavy metals serve no biological function within the cell, they can nonetheless accumulate there. Heavy metals can damage cells through two mechanisms:
- Heavy metals can increase the formation of ROS by disrupting the mitochondrial electron transport chain or by inhibiting the cells’ utilization of other metals, such as selenium.
- Heavy metals can impair the cell’s antioxidant defense by binding to sulfur-containing amino acids in proteins and to glutathione compounds.
Mercury and cadmium are known to bind strongly to sulfur-containing molecules. This can deplete cellular glutathione stores, preventing the molecule from performing its normal function optimally. They can also bind to and inhibit enzymes that rely on active cysteine or selenocysteine. Arsenic(III) can also bind to sulfur and affect redox systems and energy metabolism, thereby indirectly increasing ROS levels. Among other effects, aluminum can disrupt cellular iron handling—thereby increasing the production of free radicals—and subsequently compromise mitochondrial membranes, reducing the cell’s energy supply.
Complex antioxidant reactions
The interaction between free radicals (R•) and antioxidants is highly complex. Seven specific mechanisms have been documented by which electrons (e⁻), protons (H⁺), and entire hydrogen molecules (H•) can be transferred from an antioxidant to a free radical. In the table below, cresol is used as the antioxidant in all examples.
| Process name | Diagram of the reaction process | Antioxidant example |
| Hydrogen atom transfer (HAT) |  |
Glutathione Dihydrolipoic acids Tryptophan |
| Proton-coupled Electron Transfer (PCET) |  |
Flavonoider Curcumin (+cOOH) Vitamin E Ubiquinol |
| Single Electron Transfer (SET) |  |
Enol isomer af curcumin Galloylated tannins Planar catechin analoger Tetrahydrofuran lignans |
| Radical Adduct Formation (RAF) |  |
Carotenoider Hydroxybenzyl alcohols Rebamipide Carnosine |
| Sequential Proton Loss Electron Transfer (SPLET) |  |
Curcumin (+DDPH) Esculetin Resveratrol Piceatannol Trolox |
| Sequential Electron Transfer-Proton Transfer (SET-PT) |  |
Baicalein Astaxanthin α-Tocopherol |
| Sequential Proton Loss Hydrogen Atom Transfer (SPLHAT) |  |
Anthocyanidins Chalcone derivatives Coumarin–chalcone hybrids Betanidin |
The table has been adapted from Galano (2025), which also describes the above reactions in greater detail.
Conclusion: ‘Antioxidants’ are primarily a matter of balance and location
In small, controlled amounts, free radicals play an important role within cells, participating in normal cellular signaling and immune system functions. The problem arises when ROS concentrations become so high that cells and organs are subjected to oxidative stress, resulting in damage that the cell cannot repair in time.
Iron and copper are essential minerals, but an excess can cause severe oxidative stress. Heavy metals can both increase ROS levels and impair cellular defenses. Dietary intake of vitamins C and E is crucial, as they play distinct roles associated with water and fat, respectively.
Through our diet, we can play a significant role in protecting the body from the burden of free radicals, thereby ensuring a long and healthy life.
References and further reading
Ayala, A., Muñoz, M.F. and Argüelles, S. (2014) ‘Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal’, Oxidative Medicine and Cellular Longevity, 2014(1), p. 360438. Available at:
https://doi.org/10.1155/2014/360438
Bhattacharjee, B. et al. (2026) ‘Interplay of Reactive Oxygen Species (ROS) and Inflammatory Pathways in Diabetes’, in S. Ashique and N. Mishra (eds) Reactive Oxygen Species in Metabolic Inflammation. Cham: Springer Nature Switzerland, pp. 229–243. https://doi.org/10.1007/978-3-032-11752-6_11
Galano, A. (2025) ‘Antioxidant activity at the molecular level: exploring ways of action and computational tools to investigate them’, Chemical Science, 16(42), pp. 19570–19593. https://doi.org/10.1039/d5sc05463j
Gasparovic, A.C. et al. (2017) ‘Biomarkers of oxidativte and nitro‐oxidativte stress: conventional and novel approaches’, British Journal of Pharmacology, 174(12), pp. 1771–1783. Available at: https://doi.org/10.1111/bph.13673
Goswami, S. (2026 a) ‘Free radicals and other reactive oxygen species in human health and diseases—A historical perspective. Chapter 1’, Fundamentals of Redox Biology. Elsevier, pp. 3–26. Available at: https://doi.org/10.1016/B978-0-443-22335-8.00007-3
Goswami, S. (2026 b) ‘Role of ROS in metabolism: The cancer cell paradigm. Chapter 8’, Fundamentals of Redox Biology. Elsevier, pp. 211–230. Available at: https://doi.org/10.1016/B978-0-443-22335-8.00009-7
Goswami, S. (2026 c) ‘The role of ROS in cardiovascular and neurological disorders. Chapter 9’, Fundamentals of Redox Biology. Elsevier, pp. 231–250. Available at: https://doi.org/10.1016/B978-0-443-22335-8.00012-7
Harman, D. (1956) ‘Aging: A Theory Based on Free Radical and Radiation Chemistry’, Journal of Gerontology, 11(3), pp. 298–300. Available at: https://doi.org/10.1093/geronj/11.3.298
Jena, A. B., et al. (2023). Cellular Red-Ox system in health and disease: The latest update. Biomedicine & Pharmacotherapy, 162, 114606. https://doi.org/10.1016/j.biopha.2023.114606
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