Synergetic inhibition of the brain mitochondrial NADH: Ubiquinone oxidoreductase (Complex I) by fatty acids and Ca2

The NADH:ubiquinone oxidoreductase (respiratory complex I) activity of inside-out pig brain submitochondrial particles is inhibited by endogenous or externally added free fatty acids in time-dependent fashion. The rate and degree of the inhibition is dramatically increased by Ca 2+ . The Ca 2+ -prom...

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Bibliographic Details
Published in:Biochemistry (Moscow) 2011-08, Vol.76 (8), p.968-975
Main Authors: Kalashnikov, D. S., Grivennikova, V. G., Vinogradov, A. D.
Format: Article
Language:English
Subjects:
Animals
Biochemistry
Biomedical and Life Sciences
Biomedicine
Bioorganic Chemistry
Brain - enzymology
Brain - metabolism
Calcium - metabolism
Down-Regulation
Enzyme Inhibitors - chemistry
Enzyme Inhibitors - metabolism
Fatty Acids - metabolism
Kinetics
Life Sciences
Microbiology
Mitochondria - chemistry
Mitochondria - enzymology
NAD(P)H Dehydrogenase (Quinone) - antagonists & inhibitors
NAD(P)H Dehydrogenase (Quinone) - chemistry
NAD(P)H Dehydrogenase (Quinone) - metabolism
Swine
Ubiquinone - metabolism
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Summary:The NADH:ubiquinone oxidoreductase (respiratory complex I) activity of inside-out pig brain submitochondrial particles is inhibited by endogenous or externally added free fatty acids in time-dependent fashion. The rate and degree of the inhibition is dramatically increased by Ca 2+ . The Ca 2+ -promoted, fatty acid-induced inhibition is pH dependent, this being particularly evident at pH > 8.0. The inhibition is completely reversed by either EGTA or by bovine serum albumin (BSA). BSA prevents previously described (Kotlyar, A. B., Sled, V. D., and Vinogradov, A. D. (1992) Biochim. Biophys. Acta , 1098 , 144–150) inhibitory effect of Ca 2+ and alkaline pH on the de-active-to-active form transition of complex I. A possible mechanism of synergetic inhibition on complex I by Ca 2+ and fatty acids is discussed.
ISSN:0006-2979
1608-3040
DOI:10.1134/S000629791108013X