T3 PM Aquatic Ecotoxicology (Part 2)
Tuesday, 15 November 2005: 1:50 PM - 5:30 PM in Ballroom 3

(SHI-1117-586407) Effects of salinity on selenomethionine toxicity in Japanese medaka eggs.

Shi, D¹, Schlenk, D¹, ¹ Department of Environmental Sciences, University of California Riverside

ABSTRACT- Although mechanisms of organoselenium toxicity in fish are still unclear, previous studies have suggested that hypersaline conditions, occurring not only in estuarine ecosystems but also as a result of agricultural runoff carrying selenium and solutes (e.g., sulfate and calcium), protect against its acute toxicity in fish. Hypersaline conditions can induce expression and activity of the enzyme flavin-containing monooxygenase (FMO), which presumably plays a role in organoselenium toxicity in fish by oxidizing accumulated organoselenides to selenoxides which subsequently consume the antioxidant, gluthathione (GSH), in sensitive target tissues such as the developing embryo. Although salinity protected fish from acute toxicity, the effects on reproductive and developmental toxicity are not known. In this study, GSH and selenium concentrations in Japanese medaka eggs were determined following a 24-hour exposure of the eggs to 0.05mM selenomethionine (SeMet) under different hypersaline conditions (i.e., 4.2, 6.7, and 16.8 dS/m). The hatch-out ratios of the eggs following the treatment were also monitored. The results show that concentrations of GSH and the hatch-out ratio of the SeMet-pretreated medaka eggs decreased in a salinity dependent manner. Selenium concentrations in the eggs were however unaltered by salinity treatment, which implies that the metal tissue burden may not be a direct function of the observed toxicity as reflected by the decreasing GSH and hatch-out ratio. Instead, a significant correlation was observed between GSH and hatch-out ratios indicating oxidative stress as a potential mechanism of SeMet toxicity in fish embryos.

Key words: Salinity, Selenomethionine, Oxidative stress, Japanese medaka