Effect of complexes of precursors and modulators of coenzyme q biosynthesis on functional state of old rats' heart mitochondria
Author(s) -
О. Б. Кучменко,
Dmytro Petukhov,
Г В Донченко,
L. S. Mkhitaryan,
S. V. Tymoshchuk,
N. A. Strutynskaya,
Galyna L. Vavilova,
Vadim F. Sagach
Publication year - 2010
Publication title -
biomeditsinskaya khimiya
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.192
H-Index - 15
eISSN - 2310-6972
pISSN - 2310-6905
DOI - 10.18097/pbmc20105602244
Subject(s) - phenylarsine oxide , mitochondrion , cofactor , mitochondrial permeability transition pore , chemistry , lipid peroxidation , coenzyme q – cytochrome c reductase , enzyme , biochemistry , methionine , electron transport chain , biophysics , amino acid , biology , programmed cell death , apoptosis , cytochrome c
Our research demonstrate that ageing leads to changes in activity of electron-transporting enzyme complexes in myocardial mitochondria of old rats and to increased sensitivity of mitochondrial permeability transition pore to inductors of its opening - Ca2+ and phenylarsine oxide. We also observed activation of lipid and protein free-radical peroxidation processes. Administration of a complex of biologically active substances that included precursors and modulators of coenzyme Q biosynthesis (α-tocopherol acetate, 4-hydroxybenzoic acid, and methionine) we observed the increase in coenzyme Q content, correction of functional activity of mitochondrial electron-transport chain enzyme complexes, the decrease in intensivity of lipid and protein free-radical peroxidation in the heart and the decrease in sensitivity of mitochondrial permeability transition pore to inductors of its opening. This complex may be used to treat mitochondrial dysfunction under numerous pathologies of cardiovascular system, as well as in ageing.
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