Abstract
Mitochondria isolated from 21- to 412-day-old cardiomyopathic hamster heart show on the average a two-fold elevation of calcium in situ. Organelles from both normal and BIO 14.6 animals show a defect of oxidative phosphorylation when loaded with calcium. Mitochondria from myopathic animals accumulate less calcium than controls and show a partial inability to retain magnesium. When subjected to sucrose gradients, the mitochondria of 40% of myopathic animals yield a small extra fraction with higher calcium content and greater density. A similar fraction is seen in skeletal muscle of all cardiomyopathic hamsters. It is postulated that, in cells undergoing necrosis, a vicious cycle of mitochondrial calcium over-loading and energy depletion is underlying the terminal event of cell death.
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