Abstract
The precise mechanism of copper-induced hemolysis is not completely understood. Several hypotheses have been proposed. One states that copper ions (Cu II) may induce lipoperoxidation because of the occurrence of reactive oxygen species (Kumar et al. 1978; Barnes and Frieden 1983). These results were obtained from erythrocyte membranes or washed red cells. However, it is well known that plasma exerts an indubitable protective effect against copper-induced damage (Hiroshige 1980). So, in our study, lipoperoxidation was investigated in plasma and in whole blood incubated with different concentrations of copper for 24 h. In order to evaluate lipoperoxidation, thiobarbituric acid-reactive species (TBARS) and fluorescent chromolipids were assayed; polyunsaturated fatty acid (PUFA) profiles were studied. Recently Piriou et al. (1987) demonstrated that under air atmosphere, no lipoperoxidation occurred in red blood cells, whereas this phenomenon was evident in plasma in the presence of elevated concentrations of copper.
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References
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© 1988 Springer-Verlag
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Tallineau, C., Chahboun, S., Perault, M.C., Reiss, D., Piriou, A. (1988). Is the Noxious Hemolytic Effect of Copper a Result of Lipoperoxidation?. In: Chambers, P.L., Chambers, C.M., Dirheimer, G. (eds) The Target Organ and the Toxic Process. Archives of Toxicology, vol 12. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-73113-6_86
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DOI: https://doi.org/10.1007/978-3-642-73113-6_86
Publisher Name: Springer, Berlin, Heidelberg
Print ISBN: 978-3-540-18512-3
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