The Metabolic Fate of Mitochondrial Hydrogen Peroxide

Abstract

Mitochondrial H 2 O 2 formation is not in equilibrium with defence mechanisms that counteract an accumulation of H 2 , in rat‐heart cell. A model for the accumulation kinetics is proposed which is consistent with the data presented. Four different pathways of H 2 O 2 metabolism are described in rat‐heart mitochondria. The major site for metabolic branching of H 2 O 2 Via different routes was found to be the mitchondrial catalase. Glutathione (GSH) peroxidase accounts for only 15% of intramitochondrial H 2 O 2 metabolism, while catalase‐mediated destruction is four times more rapid. Catalase activity is limited by its structural compartmentation in the matrix, while GSH peroxidase activity was found to be dependent on the availability of free GSH. Catalase was shown to protect rat‐heart mitochondria from upsetting redox states of GSH and pyridine nucleotides following H 2 O 2 , decomposition by GSH peroxidase. Computer simulations of experimental data Suggest the existence of a third sink for mitochondrial H 2 O 2 , possibly due to mitochondrial formation of OH′ radicals; another fraction of the H 2 O 2 matrix pool may cross the mitochondrial membrane and accumulate in the cytosol.

Keywords

Affiliated Institutions

• Ludwig-Maximilians-Universität München DE

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