The modulation of thiol redox state affects the production and metabolism and hydrogen peroxide by heart mitochondrial.

In rat heart mitochondria, auranoWn, arsenite, diamide, and BCNU increase H2O2 formation, further stimulated by antimycin. However, in submitochondrial particles, H2O2 formation and oxygen uptake are not aVected, indicating that these substances do not alter respiration. Mitochondria are also able to rapidly metabolize added H2O2 in a process partially prevented by BCNU or auranoWn. Calcium does not modify the production of H2O2 and the mitochondrial thioredoxin system is not aVected by calcium ions. AuranoWn, arsenite, and diamide determine a large mitochondrial permeability transition, while BCNU and acetoacetate are ineVective. Thiols and glutathione are modiWed only by BCNU and diamide. However, all the compounds tested cause the release of cytochrome c that occurs also in the absence of mitochondrial swelling. In conclusion, the compounds utilized share the common feature of shifting the mitochondrial thiol-linked redox balance towards a more oxidized condition that is responsible of the observed eVects.