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Glucocorticoids decrease cytochrome c oxidase activity of isolated rat kidney mitochondria
Author(s) -
Simon Nicolas,
Jolliet Pascale,
Morin Christophe,
Zini Roland,
Urien Saı̈k,
Tillement Jean-Paul
Publication year - 1998
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)01033-3
Subject(s) - mitochondrion , cytochrome c oxidase , oxidative phosphorylation , cytochrome c , respiration , cytochrome , glucocorticoid , chemistry , endocrinology , medicine , kidney , respiratory chain , oxidase test , dexamethasone , biochemistry , biology , enzyme , anatomy
The importance of mitochondria is rising as a target in pathologic processes such as ischemia. We have investigated the effects of hydrocortisone, prednisolone, dexamethasone and triamcinolone on oxidative phosphorylation, Ca 2+ fluxes, swelling and membrane potentials in isolated kidney mitochondria. The measurement of respiration state 3 showed a significant decrease in presence of glucocorticoids whereas the other respiration states were not modified. When mitochondria were uncoupled and either the complexes III and IV or the complex IV were stimulated, the O 2 consumption was decreased by glucocorticoids. These results suggest the cytochrome c oxidase is a target of the glucocorticoid effect on the respiratory chain. Indeed, the other mitochondrial functions investigated were unchanged, ruling out a direct effect on Ca 2+ fluxes or swelling. A regulation of cytochrome c oxidase activity by glucocorticoids will be of particular interest in pathology involving metabolic insult.