Correction of Alcohol-Induced Damage to Mitochondria in Cardiac and Cerebral Cells by Derivatives of Neuroactive Amino Acids

We studied LPO intensity and respiration of mitochondria in brain and heart cells of rats receiving 5% ethanol for 20 weeks and treated with derivatives of neuroactive amino acids. Chronic semicompulsory alcohol intoxication increased the concentration of LPO products in cardiac and cerebral mitocho...

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Bibliographic Details
Published in:Bulletin of experimental biology and medicine 2020-06, Vol.169 (2), p.218-223
Main Authors: Popova, T. A., Khusainova, G. Kh, Prokofiev, I. I., Perfilova, V. N., Tyurenkov, I. N., Bagmetova, V. V., Malyuzhenko, I. V., Ganzikova, N. S., Dudchenko, G. P., Ostrovskii, O. V.
Format: Article
Language:English
Subjects:
Alcoholism
Antioxidants
Biological products
Biomedical and Life Sciences
Biomedicine
Cell Biology
Enzymes
Ethylenediaminetetraacetic acid
GABA
Glutamate
Internal Medicine
Laboratory Medicine
Pathology
Superoxide
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Summary:We studied LPO intensity and respiration of mitochondria in brain and heart cells of rats receiving 5% ethanol for 20 weeks and treated with derivatives of neuroactive amino acids. Chronic semicompulsory alcohol intoxication increased the concentration of LPO products in cardiac and cerebral mitochondria by 46 and 45% (diene conjugates), by 97 and 8% (diketones), and by 28 and 81% (malondialdehyde), respectively, reduced activity of antioxidant enzymes in cardiac and cerebral mitochondria by 24 and 45% (glutathione peroxidase) and by 22 and 26% (superoxide dismutase), respectively, and uncoupled the process of respiration and ATP synthesis, which manifested in a decrease in respiratory control (V 3 /V 4 ratio according to Chance ). Glutamic acid derivative Neuroglutam (26 mg/kg) and GABA derivative succicard (44 mg/kg) administered intraperitoneally daily for 28 days after termination of alcoholization decreased the levels of primary and secondary LPO products, up-regulated activity of antioxidant enzymes in mitochondria of the heart and brain, and moderated the mitochondrial dysfunction.
ISSN:0007-4888
1573-8221
DOI:10.1007/s10517-020-04854-1