Hydrogen peroxide production by monoamine oxidase during ischemia/reperfusion

Reactive oxygen species have been postulated to play a crucial role in the pathogenesis of renal ischemia-reperfusion injury. However, the intracellular sources of reactive oxygen species during ischemia-reperfusion are still unclear. In the present study, we examined whether catecholamine-degrading enzymes monoamine oxidases contribute to hydrogen peroxide (H 2O 2) generation during ischemia-reperfusion using an in vivo rat model of unilateral renal ischemia. The monoamine oxidases were characterized in homogenates of renal cortex by enzyme assay and by Western blot analysis. The monoamine oxidase-dependent H 2O 2 production was measured by luminol-amplified chemiluminescence assay. Renal monoamine oxidase activity and H 2O 2 generation by monoamine oxidases were suppressed during ischemia. The monoamine oxidase-dependent H 2O 2 production was observed during the first 15 min of reperfusion. In addition, enzyme assays showed that monoamine oxidase is also activated in this period. Rat pre-treatment with the irreversible inhibitor of monoamine oxidase, pargyline, prevented H 2O 2 production. These data suggest that monoamine oxidases are a potential source of H 2O 2 generation in the early reperfusion following ischemia, which could be involved in renal ischemia-reperfusion injury.