Acute Toxicity, Uptake and Histopathology of Aqueous Methyl Mercury to Fathead Minnow Embryos

Abstract

Early life stages of fishes have been shown to be especially susceptible to the toxic effects of heavy metal pollution. In this study, fathead minnow (Pimephales promelas) embryos were exposed in the laboratory to a graded series of aqueous methyl mercury concentrations under continuous-flow conditions. A number of toxicological endpoints were examined including; acute toxicity, bioaccumulation, protein production, impact on mitosis, gross and histopathology. Acute toxicity, reported as LC50 values of methyl mercury, ranged from 221 microg/l (95% C.I. 246-196 microg/l) for 24-h tests to 39 microg/l (95% C.I. 54-24 microg/l) for 96-h exposures. Fathead minnow embryos were shown to rapidly take up mercury from the surrounding water. Mercury levels in embryos reached levels of 2.80 microg/g wet weight after 96 h exposure to 40 microg/l methyl mercury. An initial elevation of total protein in embryo was observed in embryos exposed to 25 microg/l methyl mercury during the first 12 h of development. At later stages, significantly lower levels of protein/microg embryo were observed. Methyl mercury had no effect on mitotic stages (p=0.05) in early, cleaving blastula-stage embryos. Live embryos and serial sections were utilized to characterize changes in embryo morphology and histopathology.

Heavy metals levels in fish from aquaculture farms and risk assessment in Lhasa, Tibetan Autonomous Region of China

“…Heavy metals (such as mercury, cadmium, copper, lead, etc.) are ubiquitous and persistent contaminants in both freshwater and marine environment (Devlin 2006;Ozmen et al 2006;Macken et al 2009) and these pollutants would finally human by consuming the contaminated fish (Ramirez-Perez et al 2004;Sawasdee and Kohler 2010). Specially, cadmium is toxic to the kidney and has a long biological half-life in human, it is possible that high concentrations of cadmium can inhibit ChE activity through binding with sulfhydryl groups in or near active sites of enzymes (Silva and Pathiratne 2008).…”

Evaluating the Effects of Fly Ash Exposure on Fish Early Life Stages: Fathead Minnow Embryo-Larval Tests

“…Fish eggs, in general, are known to be capable of concentrating heavy metals and other environmental contaminants from water-borne exposures during embryonic development (Jezierska and others 2009), and fathead minnow embryos in particular have been shown to concentrate methylmercury (Devlin 2006) as well as other chemical toxicants. This technical report focuses on the responses of fathead minnow embryos to simple contact exposures to fly ash in laboratory toxicity tests adapted from a standard fathead minnow (Pimephales promelas) 7-d embryo-larval survival and teratogenicity test (method 1001.0 in EPA 2002) with mortality, hatching success, and the incidences of developmental abnormalities as measured endpoints.…”

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“…This is proved that mercury act to inhibit protein GnRH and GtH synthesis and finnaly will inhibit secretion of estradiol. Mercury poisoning lead to elevated death rate, weight loss, larvae deformation, depressed protein synthesis, hormonal imbalance, abnormal behavior, spawning reduction, sexual dysfunction, color changes, in fish (Oliviera Robeiro et al, 2002;Devline 2006;Houck and Cech 2004;Dervnick and Sandheinrich 2003;Friedmann et al, 1996). Mercury depressed protein synthesis via inhibit transcription factors for gene expression.…”

“…Naturally, the various forms of elemental, inorganic, and organic mercury are interconverted (Eisler 2004;Crespo-Lopez et al, 2007), and it has been shown that HgCl is the most poisonous form of mercury compounds (Silva-Pereira et al, 2005). Mercury poisoning lead to elevated death rate, weight loss, larvae deformation, depressed protein synthesis, hormonal imbalance, abnormal behavior, spawning reduction, sexual dysfunction, color changes, in fish (Oliviera Robeiro et al, 2002;Devline 2006;Houck and Cech 2004;Dervnick and Sandheinrich 2003;Friedmann et al, 1996).…”