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Effects of some chelating agents on the uptake and distribution of 203Hg2+ in the brown trout (Salmo trutta): studies on ethyl- and isopropylxanthate, diethyl- and diisopropyldithiophosphate, dimethyl- and diethyldithiocarbamate and pyridinethione

, : Effects of some chelating agents on the uptake and distribution of 203Hg2+ in the brown trout (Salmo trutta): studies on ethyl- and isopropylxanthate, diethyl- and diisopropyldithiophosphate, dimethyl- and diethyldithiocarbamate and pyridinethione. Archives of Toxicology 62(5): 387-391

Brown trout, Salmo trutta, were exposed to water containing 0.1 microgram/l 203Hg2+, alone or with potassium ethylxanthate (PEX), sodium isopropylxanthate (SIX), sodium diethyldithiophosphate (SEP), sodium diisopropyldithiophosphate (SIP), sodium dimethyldithiocarbamate (SMC), sodium diethyldithiocarbamate (SEC) or sodium pyridinethione (SPyr), respectively. After 1 week the uptake and distribution of the 203Hg2+ in the fish were examined by gamma spectrometry. SIX, SIP, SMC, SEC and SPyr induced 2-3 times higher 203Hg2+ concentrations in most tissues in comparison with trout exposed to 203Hg2+ only. In the trout exposed to PEX slightly enhanced 203Hg2+ levels were found only in some tissues, and after exposure to SEP a few tissues showed decreased 203Hg2+ concentrations. Determinations of chloroform/water partition coefficients showed that lipophilic chelates are formed between all the examined substances and the 203Hg2+. However, SIX, SIP, SMC, SEC and SPyr, which induced markedly increased tissue levels of the metal, formed 203Hg2+ complexes with higher lipophilicities than SEX and SEP. A facilitated penetration of the lipophilic 203Hg2+ complexes over the gill membranes may underly the increment in the tissue levels of the metal, and the relative lipophilicity of the complexes may be of importance for this effect. In some instances, as with SEP, the 203Hg2+ chelated in complexes with low lipophilicity may even be less able to acumulate in some tissues than the non-complexed metal.

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Accession: 001820099

PMID: 2853939

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