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However, Bax-deficient animals, though protected initially from hepatocyte necrosis, succumbed to liver injury at later time points due to the sustained mitochondrial oxidant stress63, suggesting that in the absence of Bax, alternate mechanisms of mitochondrial protein release are activated in the face of sustained oxidant insult

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These included reduced physical, mental, and social energy, excess adipose tissue, diminished muscle mass, diminished libido, poor bone density, higher than normal cholesterol levels, and elevated rates of cardiovascular disease