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This Article Full Text Full Text (PDF) All Versions of this Article: 293/5/E1320    most recent 00138.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Arvier, M. Articles by Ritz, P. Search for Related Content PubMed PubMed Citation Articles by Arvier, M. Articles by Ritz, P.

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

¹Institut National de la Santé et de la Recherche Médicale, Unité 694, Laboratoire de Biochimie et de Biologie Moléculaire, Centre Hospitalier Universitaire, Angers, France; and ²Université de Clermont-Ferrand EA 975, Clermont-Ferrand, France

Submitted 1 March 2007 ; accepted in final form 1 August 2007

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.

ATP production efficiency; glucocorticoids; mitochondrial proton leak