作者: Jorge L Zurita , Guillermo Repetto , Ángeles Jos , Manuel Salguero , Miguel López-Artíguez
DOI: 10.1016/J.AQUATOX.2006.11.007
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摘要: Abstract Gemfibrozil is a lipid-regulating agent widely used in patients at risk of coronary disease. Pharmaceutical products, such as gemfibrozil, are found municipal effluents and represent major source contamination. To date, there little available information about the adverse effects gemfibrozil aquatic organisms. For this reason, toxic were investigated using model systems from four trophic levels. The most sensitive system was immobilization Daphnia magna , with non-observed effect level 30 μM mean effective concentration 120 μM after 72 h, followed by inhibition bioluminescence Vibrio fischeri hepatoma fish cell line PLHC-1 growth Chlorella vulgaris . Although protein content, neutral red uptake, methylthiazol metabolization lysosomal function reduced cells, stimulations observed for function, metallothionein levels succinate dehydrogenase, glucose-6-phosphate dehydrogenase acetylcholinesterase activities. No changes ethoxyresorufin- O -deethylase activity. main morphological alterations hydropic degeneration loss cells. Modulation studies on toxicity also carried out. General antioxidants calcium chelators did not modify whereas Fe(III) chelator, membrane permeable sulphydryl-protecting compound glutathione modifying agents change toxicity. One possible mechanisms seems to be binding sulphydryl groups, including those glutathione. According result, should classified harmful However, comparing concentrations water quantified assayed systems, expected acute biota.