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- W2076280870 abstract "Previous work in our laboratory has shown that chronic ethanol ingestion induced a change in rat liver mitochondria which we termed increased fragility. This change was detected biochemically by measuring an increase in oxygen consumption during the succinic dehydrogenase assay. It was indicated ultrastructurally by swelling of the matrix compartment and loss of the outer membrane. This change was postulated to represent an acceleration of the aging process resulting from an increase in the rate of membrane phospholipid hydrolysis. In this study, the biochemical and ultrastructural changes caused by exogenous phospholipase, oleate, and lysolecithin were studied using normal liver mitochondria. The protective effects of heparin and albumin on mitochondria exposed to these agents were also studied. As was the case with the ethanol-induced fragility phenomenon, the phospholipase A induced fragility was prevented by heparin. Neither heparin nor albumin protected the mitochondria by inhibiting phospholipid hydrolysis. The effects of exogenous oleate simulated those of phospholipase A but only albumin protected the mitochondria from oleate. The evidence supports the hypothesis that the loss of mitochondrial phospholipid by hydrolysis may be the cause of the ethanol-induced fragility phenomenon and that albumin may prevent fragility by binding released fatty acids. Heparin prevents fragility by still unknown means. Studies with high amplitude phosphate swelling and contraction of the inner membrane and matrix indicated that the mitochondrial fragility phenomenon was partially reversible." @default.
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- W2076280870 date "1972-02-01" @default.
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- W2076280870 title "Effect of lipid hydrolysis and phosphate swelling on the structural and functional intergrity of mitochondria" @default.
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- W2076280870 doi "https://doi.org/10.1016/0014-4800(72)90017-2" @default.
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