Abstract

In the living cell glutathione peroxidase plays a significant role in reducing hydrogen peroxide (H2O2) as well as organic hydroperoxides. Glutathione peroxidase (selenium-dependent) activity in the heart is similar to that in liver, whereas the glutathione reductase activity is relatively low, corresponding to only 10% of the hepatic one. The redox balance of glutathione (GSH)/glutathione disulfide (GSSG) in the heart is readily shifted towards oxidation even upon a slight increase in the glutathione peroxidase reaction. It has been estimated that extra H2O2 generation in the heart with a rate exceeding only 0.4% of the oxygen consumption rate of the tissue leads to a substantial increase in the intracellular GSSG level and GSSG release from the heart. The GSSG release is considered as a sensitive indicator for the assessment of extra H2O2 generation in the heart.

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