Abstract

The role of reduction/oxidation cycling in the toxic effects of the bipyridyl herbicide paraquat was examined in the hepatopancreas of the ribbed mussel, Geukensia demissa. In vitro studies indicated a dose-dependent increase in the rate of superoxide anion (O 2 −) generation, as measured by the reduction of cytochrome c, in the microsomal fraction of the hepatopancreas. The highest concentration of paraquat employed (4 mM) elicited an 81% increase in O 2 − production above controls, which was inhibited by the addition of superoxide dismutase (SOD). For in vivo studies, a single application of paraquat (0.5, 1.0, or 2.0 mM) was added to aerated salt-water aquaria containing mussels. Biochemical analyses of antioxidant enzymes, reduced glutathione (GSH), and lipid peroxidation were performed in hepatopancreatic tissue of mussels after exposures of 6, 12, 24, and 36 h. Catalase activities were significantly elevated ( p < 0.05) in all treatment groups above controls at 6 h, in the 0.5 and 1.0 mM treatment groups at 12 h, and in the 0.5 mM group at 36 h. Total SOD activities were nearly doubled from controls in each treatment group at 12 h. However, SOD activities in exposed mussels were generally similar to or below controls at other times. GSH concentrations were generally higher in exposed mussels than in controls at all exposure periods. Lipid peroxidation in most treatment groups was significantly higher than in controls at 6, 12, and 24 h. The results support the hypotheses that these bivalves can activate redox cycling compounds and demonstrate in vivo responses typical of oxidative stress as observed in other organisms.

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