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Serum sorbitol dehydrogenase activity as an indicator of chemically induced liver damage in rainbow trout
Author(s) -
Dixon D. G.,
Hodson P. V.,
Kaiser K. L. E.
Publication year - 1987
Publication title -
environmental toxicology and chemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.1
H-Index - 171
eISSN - 1552-8618
pISSN - 0730-7268
DOI - 10.1002/etc.5620060906
Subject(s) - toxicant , rainbow trout , toxicity , biology , sorbitol dehydrogenase , histopathology , lactate dehydrogenase , medicine , endocrinology , sorbitol , physiology , andrology , toxicology , biochemistry , fish <actinopterygii> , pathology , enzyme , fishery
The utility of serum sorbitol dehydrogenase activity (SSDH) to diagnose chemically induced liver damage in fish was assessed with rainbow trout. The assay was both precise and repeatable and was unaffected by long‐term sample storage in liquid nitrogen, by fish weight, by sex, or by fasting. Exposure of trout to phenol, p ‐chlorophenol, p ‐phenoxyphenol, carbon tetrachloride, or copper injected intraperitoneally (i.p.) or added to water, caused an exposure‐dependent increase in SSDH activity. Peak activity occurred 48 h after the start of exposure. Cyanide had no effect on SSDH activity, consistent with previous observations of no hepatotoxicity. The response to toxic chemicals was unaffected by impaired liver function induced by preexposure to excessive levels of dietary carbohydrate. Elevated SSDH activity was strongly correlated to decreased serum protein levels. Hepatic lesions visible at the light‐microscope level were observed with waterborne toxicant exposure; parenchymatous edema was closely associated with increased liver somatic index (LSI). With i.p. dosing, however, biochemical lesions preceded histopathology since no visible lesions or changes in LSI were associated with toxicant exposure. Therefore, SSDH activity provides a good, reliable indicator of sublethal hepatotoxicity in studies of chemical effects on fish.