Primary causes of decreased mitochondrial oxygen consumption during metabolic depression in snail cells.

TitlePrimary causes of decreased mitochondrial oxygen consumption during metabolic depression in snail cells.
Publication TypeJournal Article
Year of Publication2002
AuthorsBishop, T, St-Pierre, J, Brand, MD
JournalAm J Physiol Regul Integr Comp Physiol
Volume282
Issue2
PaginationR372-82
Date Published2002 Feb
ISSN0363-6119
KeywordsAdenosine Triphosphate, Animals, Cell Respiration, Energy Metabolism, Estivation, Helix (Snails), Indicators and Reagents, Liver, Membrane Potentials, Mitochondria, Onium Compounds, Oxidation-Reduction, Oxygen Consumption, Pancreas, Protons, Trityl Compounds
Abstract

Cells isolated from the hepatopancreas of estivating snails (Helix aspersa) have strongly depressed mitochondrial respiration compared with controls. Mitochondrial respiration was divided into substrate oxidation (which produces the mitochondrial membrane potential) and ATP turnover and proton leak (which consume it). The activity of substrate oxidation (and probably ATP turnover) decreased, whereas the activity of proton leak remained constant in estivation. These primary changes resulted in a lower mitochondrial membrane potential in hepatopancreas cells from estivating compared with active snails, leading to secondary decreases in respiration to drive ATP turnover and proton leak. The respiration to drive ATP turnover and proton leak decreased in proportion to the overall decrease in mitochondrial respiration, so that the amount of ATP turned over per O2 consumed remained relatively constant and aerobic efficiency was maintained in this hypometabolic state. At least 75% of the total response of mitochondrial respiration to estivation was caused by primary changes in the kinetics of substrate oxidation, with only 25% or less of the response occurring through primary effects on ATP turnover.

DOI10.1152/ajpregu.00401.2001
Alternate JournalAm. J. Physiol. Regul. Integr. Comp. Physiol.
Citation Key10.1152/ajpregu.00401.2001
PubMed ID11792646