By C. J. Duncan
This quantity documents the complaints of a gathering held by means of the Society for Experimental Biology that tried to figure out no matter if there are universal mechanisms of mobile harm and to discover the ways that calcium and oxygen radicals may well have interaction to generate the wear and tear.
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Additional resources for Calcium, Oxygen Radicals and Cellular Damage (Society for Experimental Biology Seminar Series)
Such a low [Ca2+]i is maintained through the concerted action of Ca2+-translocases present in the mitochondrial, endoplasmic reticular, and the plasma membrane (Carafoli, 1987) and by Ca2+ sequestration into the nucleus as more recently proposed (Nicotera et al, 1989a; 1990) (Fig. 2). The plasma membrane translocases (which are Ca2+-ATPases in liver cells and erythrocytes, and a Na + /Ca 2+ exchanger in excitable tissues) balances the passive influx of Ca 2+ from the extracellular environment, and the Ca2+-translocating activities of mitochondria, endoplasmic reticulum, and perhaps also liver cell nuclei, contribute to the low [Ca2+ ]i?
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Menadione (2methyl-l,4-naphthoquinone)-induced Ca2+ release from rat-liver mitochondria is caused by NAD(P)H oxidation. Xenobiotica 16, 873-82. , Larsson, R. & Cerutti, P. (1988). Active oxygeninduced DNA strand breakage and poly-ADP-ribosylation in promotable and non-promotable JB6 mouse epidermal cells. Carcinogenesis 9, 239-45. Murachi, T. (1983). Intracellular Ca2+ proteases and its inhibitor protein: calpain and calpastatin. In Calcium and Cell Function vol. IV, ed. Y. Cheung, pp. 376-^10.