Molecular mechanism for aging control

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To investigate pathological role of oxidative stress on nonalcoholic steatohepatitis (NASH), we used CuZn-SOD-deficient mice, which developed spontaneous fatty liver with increased oxidative stress. Although methionine and choline-deficient (MCD) diet induced NASH-like pathologies in wild-type mice, CuZn-SOD-deficient mice failed to show typical hepatic injuries, suggesting that CuZn-SOD deficiency prevented from MCD-diet induced by hepatic stress. Furthermore, we crossbred CuZn-SOD-deficient mice with ob/ob mice to investigate pathological role of obesity on hepatic CuZn-SOD deficiency. Interestingly, double mutant mice also failed to show apparent hepatic abnormalities, suggesting that CuZn-SOD deficiency does not accelerate hepatic pathologies induced by impaired leptin signaling and obesity.