Analysis of regulatory mechanism in p66shc-mediated oxidative stress

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P66shc-deficient mice have a maximum lifespan that was up to 30% greater than that of normal mice and are less susceptible to various aging-associated diseases, such as cardiovascular diseases and diabetes, than normal mice. This study was aimed to elucidate the molecular mechanism behind this phenomenon. We revealed that cellular susceptibility to oxidative stress and ionizing radiation was regulated by p66shc. We also found that hydrogen peroxide was responsible for mediating the oxidative stress to p66shc, and that the interaction between p66shc and Heat shock protein 72 influenced the cellular radiosensitivity.