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ToxSci Advance Access published online on July 11, 2003
Toxicological Sciences, doi:10.1093/toxsci/kfg184
Toxicological Sciences © Society of Toxicology 2003; all rights reserved
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Received May 16, 2002; accepted June 24, 2003
© 2003 Society of Toxicology

Environmental Toxicology

Effects of Salinity on the Uptake, Biotransformation and Toxicity of Dietary Seleno-L-Methionine to Rainbow Trout

Daniel Schlenk 1*, Natalia Zubcov 2, and Elena Zubcov 2

1 Environmental Toxicology Program, University of California, Riverside, USA
2 Institute of Zoology, Moldovan Academy of Sciences, Chisinau, Moldova

* To whom correspondence should be addressed. E-mail: daniel.schlenk{at}ucr.edu.


  Abstract

Selenium is an element which has been of environmental concern in aquatic systems that drain arid regions heavily used for agricultural purposes. As hypersaline conditions are associated with these ecosystems, this study examined the effect of hypersaline water on the uptake, biotransformation and toxicity of seleno-L-methionine in juvenile rainbow trout. Fish were acclimated for 5 d to 4 different salinity regimes (0.5, 6.3, 11.9, 16.8 dS/m). To mimic arid agricultural runoff solutes, the water was reconstituted with ions found in drainage water of the San Joaquin River in California. Following 7 days of dietary exposure to 180 mg/kg Seleno-L-methionine (SeMe), mortality, as well as hepatic selenium concentrations and reduced: oxidized glutathione ratios were measured. Hypersaline conditions protected fish from dietary SeMe toxicity. Fish exposed to 0.5 dS/m water experienced 100% lethality in 2.5 days, whereas fish acclimated to 16.8 dS/m water only experienced 16.7% mortality which took 5-7 days to occur. There were no significant differences in hepatic selenium concentrations, but diminishment of GSH:GSSG ratios was observed in SeMe-treated fish held in 0.5 dS/m water. SeMe inhibited flavin-containing monoxygenase catalyzed trimethylamine oxidase activity, but salinity failed to induce expression in trout indicating a oxygenation of organoselenides may be a minor role in SeMe toxicity.

Key Words: selenium, selenomethionine, salinity, flavin-containing monoxygenase, glutathione, oxidative stress .


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