Oxidative stress in the pathogenesis of stroke and its correction

Martynov, M. Yu.; Журавлева, М. В.; Vasyukova, N.S.; Kuznetsova, E. V.; Каменева, Т Р

doi:10.17116/jnevro202312301116

Cited by 5 publications

(1 citation statement)

References 58 publications

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“…Because of its high and specific metabolic activity, neurons are particularly vulnerable to oxidative damage. High oxygen consumption, almost entirely oxidative phosphorylation, low energy reserves, high concentrations of peroxidizable lipids, and high levels of iron acting as prooxidants all contribute to this vulnerability [ 12 ]. As a result, neuronal cells are extremely vulnerable to metabolic/ischemic damage and the associated oxidative stress [ 13 ].…”

Section: Ros and Oxidative Stress In Strokementioning

confidence: 99%

Reverse Electron Transport at Mitochondrial Complex I in Ischemic Stroke, Aging, and Age-Related Diseases

Chavda

2023

Antioxidants

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Stroke is one of the leading causes of morbidity and mortality worldwide. A main cause of brain damage by stroke is ischemia-reperfusion (IR) injury due to the increased production of reactive oxygen species (ROS) and energy failure caused by changes in mitochondrial metabolism. Ischemia causes a build-up of succinate in tissues and changes in the mitochondrial NADH: ubiquinone oxidoreductase (complex I) activity that promote reverse electron transfer (RET), in which a portion of the electrons derived from succinate are redirected from ubiquinol along complex I to reach the NADH dehydrogenase module of complex I, where matrix NAD+ is converted to NADH and excessive ROS is produced. RET has been shown to play a role in macrophage activation in response to bacterial infection, electron transport chain reorganization in response to changes in the energy supply, and carotid body adaptation to changes in the oxygen levels. In addition to stroke, deregulated RET and RET-generated ROS (RET-ROS) have been implicated in tissue damage during organ transplantation, whereas an RET-induced NAD+/NADH ratio decrease has been implicated in aging, age-related neurodegeneration, and cancer. In this review, we provide a historical account of the roles of ROS and oxidative damage in the pathogenesis of ischemic stroke, summarize the latest developments in our understanding of RET biology and RET-associated pathological conditions, and discuss new ways to target ischemic stroke, cancer, aging, and age-related neurodegenerative diseases by modulating RET.

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Section: Ros and Oxidative Stress In Strokementioning

confidence: 99%

Reverse Electron Transport at Mitochondrial Complex I in Ischemic Stroke, Aging, and Age-Related Diseases

Chavda

2023

Antioxidants

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Effect of Cold Atmospheric Pressure Gas-Discharge Plasma on Cellular Model of Paramecium caudatum in the Study of Antioxidant Properties of Mexidol

Abrashitov,

Gruzdev,

Yakunin

et al. 2023

Phys. Atom. Nuclei

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The Antioxidant Protection System State of Rats Under Experimental Doxorubicin Intoxication and the Effects of Correcting Factors

Gutyj

Varkholiak

Verveha

et al. 2023

MCCh

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Introduction. The doxorubicin model was used for research, which, according to many authors, most adequately reproduces heart failure of varying degrees of severity. Doxorubicin is an antibiotic that has a cytostatic effect. The mechanism of its action consists of interaction with DNA, formation of free radicals, and inhibition of nucleic acid synthesis. The doxorubicin action and the development of hypoxia are accompanied by the activation of oxidative stress, the strengthening of free radical processes, and changes in the metabolism of carbohydrates, proteins, and lipids. The aim of the study – the effect of the drug “Bendamine” on the indicators of antioxidant protection of the body of rats under experimental simulation of heart failure. Research Methods. Modeling of heart failure was performed on sexually mature male Wistar rats with a body weight of 180–200 g. In blood and myocardial homogenate, the level of lipid peroxidation products, the activity of antioxidant enzymes, and the level of reduced glutathione were determined against the background of doxorubicin intoxication and when using the drug “Bendamine”. Results and Discussion. During doxorubicin intoxication, LPO processes are enhanced in rats, which is indicated by the increased lipid hydroperoxides, diene conjugates, and TBA-active products in the blood and the homogenate of the rat myocardium of the first experimental group. It is worth noting that the inhibition of the antioxidant defense system was also established in intoxicated rats, as indicated by the low level of both enzymatic and non-enzymatic links of the antioxidant system. It was established that bendamine has a corrective effect on rats' oxidative stress conditions inherent in doxorubicin-induced heart failure. The drug “Bendamine” inhibits the excessive formation of POL products in pathologically changed tissues of the heart of rats and has an inducing effect on the system of antioxidant protection. Conclusions. The influence of the drug "Bendamine" on the indicators of antioxidant protection of the body of rats under experimental simulation of heart failure was studied. Its antioxidant properties have been proven.

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Oxidative stress in the pathogenesis of stroke and its correction

Cited by 5 publications

References 58 publications

Reverse Electron Transport at Mitochondrial Complex I in Ischemic Stroke, Aging, and Age-Related Diseases

Reverse Electron Transport at Mitochondrial Complex I in Ischemic Stroke, Aging, and Age-Related Diseases

Effect of Cold Atmospheric Pressure Gas-Discharge Plasma on Cellular Model of Paramecium caudatum in the Study of Antioxidant Properties of Mexidol

The Antioxidant Protection System State of Rats Under Experimental Doxorubicin Intoxication and the Effects of Correcting Factors

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