Mitochondrial function and critical temperature in the Antarctic bivalve, Laternula elliptica

Citation
Ho. Portner et al., Mitochondrial function and critical temperature in the Antarctic bivalve, Laternula elliptica, COMP BIOC A, 124(2), 1999, pp. 179-189
Citations number
53
Categorie Soggetti
Animal Sciences",Physiology
Journal title
COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY A-MOLECULAR AND INTEGRATIVE PHYSIOLOGY
ISSN journal
10956433 → ACNP
Volume
124
Issue
2
Year of publication
1999
Pages
179 - 189
Database
ISI
SICI code
1095-6433(199910)124:2<179:MFACTI>2.0.ZU;2-7
Abstract
Thermal sensitivities of maximum respiration and proton leakage were compar ed in gill mitochondria of the Antarctic bivalve Laternula elliptica for an assessment of the contribution of mitochondrial mechanisms to limiting tem perature tolerance. Proton leakage was measured as the oxygen consumption r ate during blockage of oxidative phosphorylation (state IV respiration + ol igomycin). The maximum capacity of NADP dependent mitochondrial isocitrate dehydrogenase (IDH) was investigated as part of a proposed mitochondrial su bstrate cycle provoking proton leakage by the action of transhydrogenase. S tate III and IV + respiration rose exponentially with temperature. Thermal sensitivities of proton leakage and IDH were unusually high, in accordance with the hypothesis that H+ leakage is an enzyme catalysed process with IDH being involved. In contrast to proton leakage, state III respiration exhib ited an Arrhenius break temperature at 9 degrees C, visible as a drop in th ermal sensitivity close to, but still above the critical temperature of the species (3-6 degrees C). Progressive uncoupling of mitochondria led to a d rop in RCR values and P/O ratios at high temperature. The same discontinuit y as for state III respiration was found for the activity of mitochondrial IDH suggesting that this enzyme may influence the thermal control of mitoch ondrial respiration. In general, the high thermal sensitivity of proton lea kage may cause an excessive rise in mitochondrial oxygen demand and a decre ased efficiency of oxidative phosphorylation. This may exceed the whole ani mal capacity of oxygen uptake and distribution by ventilation and circulati on and set a thermal limit, characterized by the transition to anaerobic me tabolism. (C) 1999 Elsevier Science Inc. All rights reserved.