Abstract
Previous studies have suggested that nitric oxide (NO) inhibited mitochondrial respiration. NO and/or its intermediate(s) react with various molecules, such as hemeproteins and free SH groups. The inhibitory effect of NO on mitochondrial respiration was decreased by exogenously added glutathione (GSH). However, a decrease of intramitochondrial GSH by pretreating animals with l-buthionine sulfoximine had no appreciable effect on the inhibitory effect of isolated mitochondria. Furthermore, the effect of NO was not affected by depleting free SH residues in mitochondria by N-ethylmaleimide. These results suggest that cytosolic but not intramitochondrial GSH might be an important factor that determines the NO-dependent regulation of mitochondrial energy metabolism.
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