Section 30
Chapter 29,905

Adenine nucleotide translocator promotes oxidative phosphorylation and mild uncoupling in mitochondria after dexamethasone treatment

Arvier, M.; Lagoutte, L.ët.; Johnson, G.; Dumas, J.-F.ço.; Sion, B.; Grizard, G.; Malthièry, Y.; Simard, G.; Ritz, P.

American Journal of Physiology. Endocrinology and Metabolism 293(5): E1320-E1324


ISSN/ISBN: 0193-1849
PMID: 17698987
DOI: 10.1152/ajpendo.00138.2007
Accession: 029904955

Download citation:  

The composition of the mitochondrial inner membrane and uncoupling protein [such as adenine nucleotide translocator (ANT)] contents are the main factors involved in the energy-wasting proton leak. This leak is increased by glucocorticoid treatment under nonphosphorylating conditions. The aim of this study was to investigate mechanisms involved in glucocorticoid-induced proton leak and to evaluate the consequences in more physiological conditions (between states 4 and 3). Isolated liver mitochondria, obtained from dexamethasone-treated rats (1.5 mg.kg(-1).day(-1)), were studied by polarography, Western blotting, and high-performance thin-layer chromatography. We confirmed that dexamethasone treatment in rats induces a proton leak in state 4 that is associated with an increased ANT content, although without any change in membrane surface or lipid composition. Between states 4 and 3, dexamethasone stimulates ATP synthesis by increasing both the mitochondrial ANT and F1-F0 ATP synthase content. In conclusion, dexamethasone increases mitochondrial capacity to generate ATP by modifying ANT and ATP synthase. The side effect is an increased leak in nonphosphorylating conditions.

PDF emailed within 0-6 h: $19.90