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Heat adaptation of cultured rat cardiomyoblasts and mouse myoblasts protected these cells from damage produced by staurosporine and attenuated metabolic disturbances. Heat adaptation inhibited apoptotic, but not necrotic cell death. The mechanism of antiapoptotic adaptive protection was not associated with prevention of mitochondrial depolarization, because heat adaptation not only induced depolarization of mitochondria, but also intensified this process under conditions of staurosporine-induced damage. |
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