Abstract
In vitro rat liver microsomes free of Fe2+ ions peroxidize minimally at 37° when NADPH and either CC14 or BrCC13 are added. Although the lipid peroxidation dependent on toxigenic haloalkanes in these Fe2+-free microsome systems is very low, it is considerably more efficient in causing loss of cytochrome P-450 and glucose6-phosphatase than is the far more vigorous lipid peroxidation dependent on presence of Fe2+ ions. In particular, the Ca2+-pump activity of isolated microsomes was almost completely destroyed when malonic dialdehyde (MDA) production was as little as 8 pg per gram equivalent microsomes. Moore et al. (1976) had shown previously that the capacity of liver microsomes to sequester Ca2+ was severely depressed 30 min after CC14 administration to rats. We have shown that this effect is already manifested within 3 min after CC14 administration, by which time peroxidative decomposition of microsomal lipids can be detected. The time course of the destruction of the liver microsomal Ca2+ pump after CC14 administration to rats was essentially identical to the time course of microsomal lipid peroxidation, as revealed by the appearance of conjugated diene configurations in microsomal lipids.
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Recknagel, R.O., Lowrey, K., Waller, R.L., Glende, E.A. (1982). Destruction of Microsomal Calcium Pump Activity: A Possible Secondary Mechanism in BrCCl3 and CCl4 Liver Cell Injury. In: Snyder, R., et al. Biological Reactive Intermediates—II. Advances in Experimental Medicine and Biology, vol 136. Springer, New York, NY. https://doi.org/10.1007/978-1-4757-0674-1_45
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DOI: https://doi.org/10.1007/978-1-4757-0674-1_45
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