There is also evidence that the scavenging of NO by oxygen radicals produces peroxynitrite that causes tubule damage during ischemia (58–60). The administration of α-melanocyte–stimulating hormone (αMSH) affords protection against ischemic/reperfusion renal injury by blocking both the induction of iNOS and leukocyte infiltration into the kidney during ischemia (61). Oxygen radical scavengers, such as superoxide dismutase, have also been shown to protect against acute renal injury associated with endotoxemia (62). Caspase inhibitors, IL-18 antibodies, and caspase-1 knockout mice have also been shown to be protective against ischemia/reperfusion injury (63, 64).