Inhibition of IL-1beta secretion and mitochondria respiration by arsenite which acts on myocardial ischemia-reperfusion injury

Abstract

Arsenite (NaAsO2) is a potent toxin that significantly contributes to human pathogenesis. Chronic exposure to arsenite results in various diseases. The physiologically important biological target(s) of arsenite exposure is largely unknown. Here we found that transient sodium arsenite treatment (1) blocks nigericin or Rotenone induced IL-1{beta} secretion; (2) inhibits mitochondrial respiration with complex I-linked substrate; (3) induces Heme oxygenase-1 (HO-1) in myocardial tissue. (4) attenuates the myocardial ischemia-reperfusion injury in an in vivo model of rats. The causal relationship among these activities needs further investigation.