Exposure of the frog Rana ridibunda to copper: Impact on two biomarkers, lipid peroxidation, and glutathione

摘要

Copper (Cu) is an essential trace element and it is not a potent liver toxin except in certain cases of genetic defects resulting in the inability to excrete Cu. However very high Cu intake can result in liver damage (Stemleib 1980). The effects ofthe metal overload prompted research into the mechanisms of its toxicity. When in excess "free" Cu can catalyse the production of the highly toxic hydroxyl radicals from intracellularly generated hydrogen peroxide. Oxidative stress may produce DNA damage, enzymatic inactivation and preoccupation of cell constituents, especially lipid peroxidation (Halliwell and Gutteridge 1989). Glutathione (GSH), the most abundant cellular thiol, is involved in metabolic and transport processes and in the protection ofcells against the toxic effects (Meister and Anderson 1983). GSH has been shown to form GS-Me complexes with various metals, through its thiolate sulfur atom (Rabestein et al. 1985). In light of these studies, it has been proposed that GSH is capable ofcomplexing and detoxifying heavy metal cations soon after they enter the cell, thus representing a first line of defence against heavy metal cytotoxicity (Singhal et al. 1987; Freedman et al. 1989; Naganuma et al. 1990).