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Article ; Online: Phenoptosis as a Phenomenon Widespread among Many Groups of Living Organisms Including Mammals (Commentary to the Paper by E. R. Galimov, J. N. Lohr, and D. Gems (2019) Biochemistry (Moscow), 84, 1433-1437).

Skulachev, V P

2020 Volume 84, Issue 12, Page(s) 1438–1441

Abstract: Author congratulates David Gems and co-authors on a brilliant discovery - direct proof of acute phenoptosis in the nematode - but argues that the authors underappreciate the significance of their work by suggesting that phenoptosis is a rare natural ... ...

Abstract	Author congratulates David Gems and co-authors on a brilliant discovery - direct proof of acute phenoptosis in the nematode - but argues that the authors underappreciate the significance of their work by suggesting that phenoptosis is a rare natural phenomenon not typically observed in mammals.
MeSH term(s)	Adaptation, Physiological ; Animals ; Mammals ; Moscow
Language	English
Publishing date	2020-01-15
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	1109-5
ISSN	1608-3040 ; 0006-2979 ; 0320-9717
ISSN (online)	1608-3040
ISSN	0006-2979 ; 0320-9717
DOI	10.1134/S0006297919120022
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Article ; Online: Programmed Aging of Mammals: Proof of Concept and Prospects of Biochemical Approaches for Anti-aging Therapy.

Skulachev, M V / Skulachev, V P

Biochemistry. Biokhimiia

2017 Volume 82, Issue 12, Page(s) 1403–1422

Abstract: ... prolongation of youth by deceleration of late ontogeny (Skulachev, V. P. (2015) Abst. 11th Conf ... on Mitochondrial Physiology (MiP2015), Lucni Bouda, Czech Republic, pp. 64-66; Skulachev, V. P., Holtze, S ... Vyssokikh, M. Y., Bakeeva, L. E., Skulachev, M. V., Markov, A. V., Hildebrandt, T. B., and Sadovnichii, V ...

Abstract	(i) In 2015-2017 we compared possible reasons for longevity of two mammalian highly social species, i.e. naked mole rats and humans. We proposed that in both cases longevity is a result of neoteny, prolongation of youth by deceleration of late ontogeny (Skulachev, V. P. (2015) Abst. 11th Conf. on Mitochondrial Physiology (MiP2015), Lucni Bouda, Czech Republic, pp. 64-66; Skulachev, V. P., Holtze, S., Vyssokikh, M. Y., Bakeeva, L. E., Skulachev, M. V., Markov, A. V., Hildebrandt, T. B., and Sadovnichii, V. A. (2017) Physiol. Rev., 97, 699-720). Both naked mole rats and humans strongly decreased the pressure of natural selection, although in two different manners. Naked mole rats preferred an "aristocratic" pathway when reproduction (and, hence, involvement in evolution) is monopolized by the queen and her several husbands. Huge number of subordinates who have no right to take part in reproduction and hence in evolution serves the small queen's family. Humans used an alternative, "democratic" pathway, namely technical progress facilitating adaptation to the changing environmental conditions. This pathway is open to all humankind. (ii) As a result, aging as a mechanism increasing evolvability by means of facilitation of natural selection became unnecessary for naked mole rats and humans due to strong attenuation of this selection. This is apparently why aging became a counterproductive atavism for these two species and was strongly shifted to late ages. This shift is direct evidence of the hypothesis that aging is programmed, being the last step of late ontogeny. (iii) Further deceleration of aging for humans by means of neoteny is unrealistic since the development of neoteny probably takes million years. (iv) However, if biological aging is a program, an alternative and much simpler way to avoid it seems possible. We mean inhibition of an essential step of this program. (v) At present, the most probable scheme of the aging program assumes that it is a mechanism of slow poisoning of an organism by reactive oxygen species produced by mitochondria. If this is the case, a mitochondria-targeted antioxidant might be an inhibitor of the aging program. During the last 12 years, such an antioxidant, namely SkQ1, was synthesized and studied in detail in our group. It consists of plastoquinone and decyltriphenylphosphonium (a penetrating cation responsible for electrophoretic accumulation of SkQ1 in mitochondria). It was shown that long-term treatment with SkQ1 increased the lifespan of plants, fungi, invertebrates, fish, and mammals. Moreover, SkQ1 is effective in the therapy of various age-related diseases. It was also shown that a single SkQ1 injection could save life in certain models of sudden death of animals. (vi) A tentative scheme is proposed considering aging as a process of chronic phenoptosis, which eventually results in initiation of acute phenoptosis and death. This scheme also suggests that under certain conditions chronic phenoptosis can be neutralized by an anti-aging program that is activated by food restriction regarded by an organism as a signal of starvation. As for acute phenoptosis, it is apparently controlled by receptors responsible for measuring key parameters of homeostasis. The first experimental indications have been already obtained indicating that both chronic and acute phenoptosis are suppressed by SkQ1.
MeSH term(s)	Aging/drug effects ; Aging/physiology ; Animals ; Antioxidants/pharmacology ; Humans ; Longevity/drug effects ; Mitochondria/metabolism ; Mole Rats ; Plastoquinone/analogs & derivatives ; Plastoquinone/pharmacology ; Reactive Oxygen Species/metabolism
Chemical Substances	10-(6'-plastoquinonyl)decyltriphenylphosphonium ; Antioxidants ; Reactive Oxygen Species ; Plastoquinone (OAC30J69CN)
Language	English
Publishing date	2017-12
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1109-5
ISSN	1608-3040 ; 0006-2979 ; 0320-9717
ISSN (online)	1608-3040
ISSN	0006-2979 ; 0320-9717
DOI	10.1134/S000629791712001X
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Article ; Online: Neotenic Traits in Heterocephalus glaber and Homo sapiens.

Popov, N A / Skulachev, V P

Biochemistry. Biokhimiia

2019 Volume 84, Issue 12, Page(s) 1484–1489

Abstract: The data on the neoteny (prolongation of youth and retardation of aging) in naked mole rat (Heterocephalus glaber) and Homo sapiens are summarized. Fifty-eight neotenic traits have been described by now in the naked mole rat at the organismal, tissue, ... ...

Abstract	The data on the neoteny (prolongation of youth and retardation of aging) in naked mole rat (Heterocephalus glaber) and Homo sapiens are summarized. Fifty-eight neotenic traits have been described by now in the naked mole rat at the organismal, tissue, cellular, and metabolism levels. Among them, there are traits that increase the lifespan, including mild depolarization of mitochondria that prevents generation by these organelles of reactive oxygen species known to strongly promote aging. Mild mitochondrial depolarization disappears with age in short-lived mammals (mouse Mus musculus) much faster than in long-lived mammals (e.g., naked mole rats and bats). The development of neoteny in naked mole rats has been due to the social organization. These animals live in subterranean colonies, where sexual reproduction is monopolized by the queen and one or several males who are defended and provided with nutrition by numerous subordinates. Humans have achieved a gradual increase in the lifespan first due to neoteny, and then to the technical progress, which can be observed by comparing the lifespan curves of chimpanzees, hunter-gatherers of the Paraguayan Ache tribe, and residents of Sweden from the XVII century to the present day. Significantly different rates of neoteny and technical progress make it possible to discriminate between the contributions of these two longevity mechanisms.
MeSH term(s)	Aging/genetics ; Animals ; Genome, Human ; Humans ; Longevity ; Membrane Potential, Mitochondrial ; Mitochondria/metabolism ; Mole Rats/genetics ; Reactive Oxygen Species/metabolism
Chemical Substances	Reactive Oxygen Species
Language	English
Publishing date	2019-12-20
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1109-5
ISSN	1608-3040 ; 0006-2979 ; 0320-9717
ISSN (online)	1608-3040
ISSN	0006-2979 ; 0320-9717
DOI	10.1134/S0006297919120071
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Article ; Online: Six Functions of Respiration: Isn't It Time to Take Control over ROS Production in Mitochondria, and Aging Along with It?

Skulachev, Vladimir P / Vyssokikh, Mikhail Yu / Chernyak, Boris V / Mulkidjanian, Armen Y / Skulachev, Maxim V / Shilovsky, Gregory A / Lyamzaev, Konstantin G / Borisov, Vitaliy B / Severin, Fedor F / Sadovnichii, Victor A

International journal of molecular sciences

2023 Volume 24, Issue 16

Abstract: Cellular respiration is associated with at least six distinct but intertwined biological functions. (1) biosynthesis of ATP from ADP and inorganic phosphate, (2) consumption of respiratory substrates, (3) support of membrane transport, (4) conversion of ... ...

Abstract	Cellular respiration is associated with at least six distinct but intertwined biological functions. (1) biosynthesis of ATP from ADP and inorganic phosphate, (2) consumption of respiratory substrates, (3) support of membrane transport, (4) conversion of respiratory energy to heat, (5) removal of oxygen to prevent oxidative damage, and (6) generation of reactive oxygen species (ROS) as signaling molecules. Here we focus on function #6, which helps the organism control its mitochondria. The ROS bursts typically occur when the mitochondrial membrane potential (MMP) becomes too high, e.g., due to mitochondrial malfunction, leading to cardiolipin (CL) oxidation. Depending on the intensity of CL damage, specific programs for the elimination of damaged mitochondria (mitophagy), whole cells (apoptosis), or organisms (phenoptosis) can be activated. In particular, we consider those mechanisms that suppress ROS generation by enabling ATP synthesis at low MMP levels. We discuss evidence that the mild depolarization mechanism of direct ATP/ADP exchange across mammalian inner and outer mitochondrial membranes weakens with age. We review recent data showing that by protecting CL from oxidation, mitochondria-targeted antioxidants decrease lethality in response to many potentially deadly shock insults. Thus, targeting ROS- and CL-dependent pathways may prevent acute mortality and, hopefully, slow aging.
MeSH term(s)	Animals ; Reactive Oxygen Species ; Respiration ; Mitochondria ; Aging ; Cardiolipins ; Adenosine Triphosphate ; Mammals
Chemical Substances	Reactive Oxygen Species ; Cardiolipins ; Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2023-08-08
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms241612540
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Article ; Online: New data on programmed aging - slow phenoptosis.

Skulachev, M V / Skulachev, V P

Biochemistry. Biokhimiia

2014 Volume 79, Issue 10, Page(s) 977–993

Abstract: This review summarizes the latest data on biochemistry and physiology of living organisms. These data suggest that aging, i.e. coordinated age-dependent weakening of many vital functions leading to gradual increase in the probability of dying, is not ... ...

Abstract	This review summarizes the latest data on biochemistry and physiology of living organisms. These data suggest that aging, i.e. coordinated age-dependent weakening of many vital functions leading to gradual increase in the probability of dying, is not common to all organisms. Some species have been described whose probability of death does not depend on age or even decreases with age, this being accompanied by constant or increasing fertility. In the case of the naked mole rat (a non-aging mammal), a mechanism has been identified that protects this animal from cancer and the most common age-related diseases. The high molecular weight polysaccharide hyaluronan, a linear polymer composed of multiple repeated disaccharide of glucuronic acid and glucosamine, plays the key role in this mechanism. Hyaluronan is accumulated in the intercellular spaces in the organs and tissues of the naked mole rat. This polysaccharide provides early contact inhibition of cell division (anti-cancer effect). In addition, hyaluronan prevents the development of certain types of apoptosis, in particular, those induced by reactive oxygen species (ROS) (geroprotective effect preventing ROS-induced decrease in cellularity in the organs and tissues of aging organisms). Extraordinary longevity of the naked mole rat (over 30 years, which is long for a rodent the size of a mouse) is connected to its eusocial lifestyle, when only the "queen" and its few "husbands" breed, while the huge army of non-breeding "subordinates" provide the "royal family" with protection from predators, food, and construction and maintenance of an underground labyrinth size of a football field. This way of life removes the pressure of natural selection from the "family" and makes aging - the program that is counterproductive for the individual but increases "evolvability" of its offspring - unnecessary. The example of the naked mole rat demonstrates the optional character of the aging program for the organism. Many facts indicating that aging can be regulated by an organism provide another argument in favor of optionality of aging. Cases have been described when aging as a program useful for the evolution of offspring but counterproductive for the parental individual slows under conditions that threaten the very existence of the individual. These conditions include food restriction (the threat of death from starvation), heavy muscular work, decrease or increase in the environmental temperature, small amounts of poisons (including ROS; here we speak about the paradoxical geroprotective effect of the low doses of prooxidants that inhibit apoptosis). On the other hand, aging can be inhibited (and maybe even cancelled) artificially. This can be done by turning off the genes encoding the proteins participating in the aging program, such as FAT10, p66shc, and some others. In addition, the gene of the antioxidant enzyme catalase can be addressed into mitochondria, where it will split mitochondrial hydrogen peroxide, the level of which increases with age. However, today the simplest way to slow down the aging program is the use of mitochondria-targeted low molecular weight antioxidant compounds of plastoquinonyl decyltriphenylphosphonium-type (SkQ1), which prolong the life of animals, plants, and fungi and inhibit the development of many age-related diseases and symptoms.
MeSH term(s)	Aging/physiology ; Animals ; Antioxidants/metabolism ; Apoptosis ; Biological Evolution ; Fertility ; Gene Expression Regulation ; Hyaluronic Acid/metabolism ; Invertebrates/physiology ; Longevity ; Mitochondria/metabolism ; Neoplasms/etiology ; Oxidative Stress ; Reactive Oxygen Species/metabolism ; Rodentia/physiology
Chemical Substances	Antioxidants ; Reactive Oxygen Species ; Hyaluronic Acid (9004-61-9)
Language	English
Publishing date	2014-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1109-5
ISSN	1608-3040 ; 0006-2979 ; 0320-9717
ISSN (online)	1608-3040
ISSN	0006-2979 ; 0320-9717
DOI	10.1134/S0006297914100010
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Article ; Online: Mitochondrion-targeted antioxidant SkQ1 prevents rapid animal death caused by highly diverse shocks.

Skulachev, V P / Vyssokikh, M Yu / Chernyak, B V / Averina, O A / Andreev-Andrievskiy, A A / Zinovkin, R A / Lyamzaev, K G / Marey, M V / Egorov, M V / Frolova, O J / Zorov, D B / Skulachev, M V / Sadovnichii, V A

Scientific reports

2023 Volume 13, Issue 1, Page(s) 4326

Abstract: The response to stress involves the activation of pathways leading either to protection from the stress origin, eventually resulting in development of stress resistance, or activation of the rapid death of the organism. Here we hypothesize that ... ...

Abstract	The response to stress involves the activation of pathways leading either to protection from the stress origin, eventually resulting in development of stress resistance, or activation of the rapid death of the organism. Here we hypothesize that mitochondrial reactive oxygen species (mtROS) play a key role in stress-induced programmed death of the organism, which we called "phenoptosis" in 1997. We demonstrate that the synthetic mitochondria-targeted antioxidant SkQ1 (which specifically abolishes mtROS) prevents rapid death of mice caused by four mechanistically very different shocks: (a) bacterial lipopolysaccharide (LPS) shock, (b) shock in response to intravenous mitochondrial injection, (c) cold shock, and (d) toxic shock caused by the penetrating cation C
MeSH term(s)	Mice ; Animals ; Antioxidants/pharmacology ; Antioxidants/metabolism ; Mitochondria/metabolism ; Cytokines/metabolism ; Reactive Oxygen Species/metabolism ; Plastoquinone/pharmacology ; Plastoquinone/metabolism
Chemical Substances	Antioxidants ; Cytokines ; Reactive Oxygen Species ; Plastoquinone (OAC30J69CN)
Language	English
Publishing date	2023-03-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-31281-9
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Article ; Online: Age-Dependent Changes in the Production of Mitochondrial Reactive Oxygen Species in Human Skeletal Muscle.

Vyssokikh, Mikhail Yu / Vigovskiy, Maksim A / Philippov, Vladislav V / Boroday, Yakov R / Marey, Mariya V / Grigorieva, Olga A / Vepkhvadze, Tatiana F / Kurochkina, Nadezhda S / Manukhova, Ludmila A / Efimenko, Anastasiya Yu / Popov, Daniil V / Skulachev, Vladimir P

Biochemistry. Biokhimiia

2024 Volume 89, Issue 2, Page(s) 299–312

Abstract: A decrease in muscle mass and its functionality (strength, endurance, and insulin sensitivity) is one of the integral signs of aging. One of the triggers of aging is an increase in the production of mitochondrial reactive oxygen species. Our study was ... ...

Abstract	A decrease in muscle mass and its functionality (strength, endurance, and insulin sensitivity) is one of the integral signs of aging. One of the triggers of aging is an increase in the production of mitochondrial reactive oxygen species. Our study was the first to examine age-dependent changes in the production of mitochondrial reactive oxygen species related to a decrease in the proportion of mitochondria-associated hexokinase-2 in human skeletal muscle. For this purpose, a biopsy was taken from m. vastus lateralis in 10 young healthy volunteers and 70 patients (26-85 years old) with long-term primary arthrosis of the knee/hip joint. It turned out that aging (comparing different groups of patients), in contrast to inactivity/chronic inflammation (comparing young healthy people and young patients), causes a pronounced increase in peroxide production by isolated mitochondria. This correlated with the age-dependent distribution of hexokinase-2 between mitochondrial and cytosolic fractions, a decrease in the rate of coupled respiration of isolated mitochondria and respiration when stimulated with glucose (a hexokinase substrate). It is discussed that these changes may be caused by an age-dependent decrease in the content of cardiolipin, a potential regulator of the mitochondrial microcompartment containing hexokinase. The results obtained contribute to a deeper understanding of age-related pathogenetic processes in skeletal muscles and open prospects for the search for pharmacological/physiological approaches to the correction of these pathologies.
MeSH term(s)	Humans ; Adult ; Middle Aged ; Aged ; Aged, 80 and over ; Reactive Oxygen Species/metabolism ; Hexokinase/metabolism ; Mitochondria ; Muscle, Skeletal/metabolism ; Aging/physiology ; Mitochondria, Muscle/metabolism
Chemical Substances	Reactive Oxygen Species ; Hexokinase (EC 2.7.1.1)
Language	English
Publishing date	2024-03-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	1109-5
ISSN	1608-3040 ; 0006-2979 ; 0320-9717
ISSN (online)	1608-3040
ISSN	0006-2979 ; 0320-9717
DOI	10.1134/S0006297924020093
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Article ; Online: Mitochondrial Genome and Longevity.

Zinovkin, R A / Skulachev, M V / Skulachev, V P

Biochemistry. Biokhimiia

2016 Volume 81, Issue 12, Page(s) 1401–1405

Abstract: The mitochondrial genome provides not only respiratory chain function, but it also ensures the impact of mitochondria on nearly all crucial metabolic processes. It is well known that mitochondria regulate aging and lifespan. However, until now there were ...

Abstract	The mitochondrial genome provides not only respiratory chain function, but it also ensures the impact of mitochondria on nearly all crucial metabolic processes. It is well known that mitochondria regulate aging and lifespan. However, until now there were no direct experimental data concerning the influence of various mitochondrial DNA variants on lifespan of animals with identical nuclear genome. In a recent paper of J. A. Enríquez and coworkers (Latorre-Pellicer, A., et al. (2016) Nature, 535, 561-565), it was shown that mice carrying nuclear DNA from one strain and mitochondrial DNA from another had longer median lifespan and retarded development of various aging traits. This review critically analyzes that paper and considers some aspects of the crosstalk between the nuclear and mitochondrial genomes. We also discuss new perspectives of gerontology in the light of the discovery made by Enríquez's group.
MeSH term(s)	Aging ; Animals ; DNA, Mitochondrial ; Evolution, Molecular ; Genetic Association Studies ; Genome, Mitochondrial ; Humans ; Longevity/genetics ; Reactive Oxygen Species
Chemical Substances	DNA, Mitochondrial ; Reactive Oxygen Species
Language	English
Publishing date	2016-12
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1109-5
ISSN	1608-3040 ; 0006-2979 ; 0320-9717
ISSN (online)	1608-3040
ISSN	0006-2979 ; 0320-9717
DOI	10.1134/S0006297916120014
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Article ; Online: What is "phenoptosis" and how to fight it?

Skulachev, V P

Biochemistry. Biokhimiia

2012 Volume 77, Issue 7, Page(s) 689–706

Abstract: Phenoptosis is the death of an organism programmed by its genome. Numerous examples of phenoptosis are described in prokaryotes, unicellular eukaryotes, and all kingdoms of multicellular eukaryotes (animals, plants, and fungi). There are very ... ...

Abstract	Phenoptosis is the death of an organism programmed by its genome. Numerous examples of phenoptosis are described in prokaryotes, unicellular eukaryotes, and all kingdoms of multicellular eukaryotes (animals, plants, and fungi). There are very demonstrative cases of acute phenoptosis when actuation of a specific biochemical or behavioral program results in immediate death. Rapid (taking days) senescence of semelparous plants is described as phenoptosis controlled by already known genes and mediated by toxic phytohormones like abscisic acid. In soya, the death signal is transmitted from beans to leaves via xylem, inducing leaf fall and death of the plant. Mutations in two genes of Arabidopsis thaliana, required for the flowering and subsequent formation of seeds, prevent senescence, strongly prolonging the lifespan of this small semelparous grass that becomes a big bush with woody stem, and initiate substitution of vegetative for sexual reproduction. The death of pacific salmon immediately after spawning is surely programmed. In this case, numerous typical traits of aging, including amyloid plaques in the brain, appear on the time scale of days. There are some indications that slow aging of higher animals and humans is also programmed, being the final step of ontogenesis. It is assumed that stepwise decline of many physiological functions during such aging increases pressure of natural selection on organisms stimulating in this way biological evolution. As a working hypothesis, the biochemical mechanism of slow aging is proposed. It is assumed that mitochondria-generated reactive oxygen species (ROS) is a tool to stimulate apoptosis, an effect decreasing with age the cell number (cellularity) of organs and tissues. A group of SkQ-type substances composed of plastoquinone and a penetrating cation were synthesized to target an antioxidant into mitochondria and to prevent the age-linked rise of the mitochondrial ROS level. Such targeting is due to the fact that mitochondria are the only cellular organelles that are negatively charged compared to the cytosol. SkQs are shown to strongly decrease concentration of ROS in mitochondria, prolong lifespan of fungi, invertebrates, fish, and mammals, and retard appearance of numerous traits of aging. Clinical trials of SkQ1 (plastoquinonyl decyltriphenylphosphonium) have been successfully completed so that the Ministry of Health of the Russian Federation recommends drops of very dilute (0.25 µM) solution of this antioxidant as a medicine to treat the syndrome of dry eye, which was previously considered an incurable disease developing with age. These drops are already available in drugstores. Thus, SkQ1 is the first mitochondria-targeted drug employed in medical practice.
MeSH term(s)	Aging/genetics ; Animals ; Apoptosis/genetics ; Biological Evolution ; Caloric Restriction ; Death ; Genome/genetics ; Humans ; Mitochondria/metabolism ; Reactive Oxygen Species/metabolism
Chemical Substances	Reactive Oxygen Species
Language	English
Publishing date	2012-07
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1109-5
ISSN	1608-3040 ; 0006-2979 ; 0320-9717
ISSN (online)	1608-3040
ISSN	0006-2979 ; 0320-9717
DOI	10.1134/S0006297912070012
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Article ; Online: Perspectives of

Skulachev, Vladimir P / Shilovsky, Gregory A / Putyatina, Tatyana S / Popov, Nikita A / Markov, Alexander V / Skulachev, Maxim V / Sadovnichii, Victor A

Aging

2020 Volume 12, Issue 6, Page(s) 5566–5584

Abstract: ... Homo ... ...

Abstract	Homo sapiens
MeSH term(s)	Aging/physiology ; Animals ; Female ; Humans ; Longevity/physiology ; Male ; Mole Rats/physiology ; Reactive Oxygen Species
Chemical Substances	Reactive Oxygen Species
Language	English
Publishing date	2020-03-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.102981
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