Toxicological interactions of chlorpyrifos and methyl mercury in the amphipod, Hyalella azteca

被引:36
作者
Steevens, JA
Benson, WH
机构
[1] Univ Mississippi, Sch Pharm, Dept Pharmacol, University, MS 38677 USA
[2] Univ Mississippi, Sch Pharm, Dept Environm & Community Hlth Res, University, MS 38677 USA
关键词
chemical mixture; Hyalella azteca; chlorpyrifos; methyl mercury; acetylcholinesterase; chemical interaction;
D O I
10.1093/toxsci/52.2.168
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
The mechanism of interaction between chlorpyrifos, an organophosphate insecticide, and methyl mercury, an organometal, was assessed utilizing the amphipod, Hyalella azteca. Previous studies have demonstrated that chlorpyrifos and methyl mercury interact additively, with survival as the endpoint, In addition, exposure to chlorpyrifos and methyl mercury increased the accumulation and decreased the elimination of methyl mercury. To elucidate the mechanism responsible for these interactions, biochemical mechanisms indicative of chlorpyrifos and methyl mercury toxicity were assessed in H. azteca, Biochemical endpoints that were evaluated include the inhibition of acetylcholinesterase enzyme and indicators of oxidative stress such as glutathione-S-transferase activity, lipid peroxidation, protein oxidation, and glutathione content. Methyl mercury antagonized the effects of chlorpyrifos in vivo on acetylcholinesterase inhibition. Methyl mercury did not induce oxidative damage; however, chlorpyrifos decreased glutathione-S-transferase activity. Additional studies demonstrated that methyl mercury did not affect the in vitro bioactivation of chlorpyrifos or the subsequent inhibition of acetylcholinesterase enzyme activity. Chemical-chemical interactions were examined utilizing chromatographic techniques. Results of thin layer chromatography suggested the formation of a chlorpyrifos-methyl mercury complex. The formation of this complex may result in increased accumulation of methyl mercury, apparent additive toxicity, and protection against chlorpyrifos mediated acetylcholinesterase inhibition.
引用
收藏
页码:168 / 177
页数:10
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