Abstract

Microcystin-LR (MCLR) is one of the most common toxins in eutrophic freshwater ecosystems. The ecotoxicological effects of MCLR in freshwater ecosystems have been widely documented; however, the physiological effects of MCLR on freshwater snails and the underlying toxicity/detoxification mechanisms have not been well investigated. In this laboratory study, antioxidant system responses in the hepatopancreas and the digestive tract of Radix swinhoei, a typical freshwater snail, exposed to 0.01mg/L to 2mg/L MCLR were explored. Antioxidant enzymes, particularly superoxide dismutase (SOD), catalase (CAT), and peroxidase (POD), in the digestive tracts were effectively generated at 0.2 and 2mg/L MCLR. However, SOD and CAT activities in the hepatopancreas were activated only at 0.2mg/L MCLR. Glutathione (GSH) concentrations in the digestive tracts significantly increased at 0.01 to 0.2mg/L MCLR; by comparison, GSH concentrations in the hepatopancreas remained stable. No oxidative damage (lipid peroxidations) occurred in the digestive tracts and the hepatopancreas when the snail was exposed to ≤0.2mg/L MCLR. MCLR accumulation in different snail tissues was also examined. MCLR accumulated in different tissues and showed the following pattern: hepatopancreas > gonads > digestive tracts > muscles. Bioaccumulated concentrations in these four tissues increased as MCLR exposure concentrations increased; by contrast, bioaccumulation factors decreased as MCLR exposure concentrations increased. Our results indicated that R. swinhoei is sensitively responsive to MCLR by changing antioxidant system status to cope with the toxicity. Snails may be vectors of MCs that transfer MCs in eutrophic lakes via food chains or food web.

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