Retinoic acid hydroxylation in rainbow trout ( Oncorhynchus mykiss) and the effect of a coplanar PCB, 3,3′,4,4′-tetrachlorobiphenyl

When liver microsomes of rainbow trout ( Oncorhynchus mykiss) were incubated with [ 14C]-labeled retinoic acid plus NADPH, high performance liquid chromatography revealed the presence of radioactive peaks having elution times identical to those of 4-hydroxy- and 4-oxoretinoic acid. In the absence of...

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Published inAquatic toxicology Vol. 32; no. 2; pp. 177 - 187
Main Authors Gilbert, Nicolas L., Cloutier, Marie-Josée, Spear, Philip A.
Format Journal Article
LanguageEnglish
Published Amsterdam Elsevier B.V 1995
Elsevier Science
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Summary:When liver microsomes of rainbow trout ( Oncorhynchus mykiss) were incubated with [ 14C]-labeled retinoic acid plus NADPH, high performance liquid chromatography revealed the presence of radioactive peaks having elution times identical to those of 4-hydroxy- and 4-oxoretinoic acid. In the absence of NADPH, the radioactive peaks were not detected which is consistent with cytochrome P450-dependent 4-hydroxylation. In trout injected intraperitoneally with 5 μg/g of 3,3′,4,4′-tetrachlorobiphenyl (TCB) and sacrificed 56 days later, the hydroxylation rate was higher ( P < 0.0005) compared with control trout. No difference was observed between TCB-treated and control groups 7 days after injection. In contrast, cytochrome P4501-dependent ethoxyresorufin- O-deethylase activity was significantly higher in the TCB-treated group, both at 7 and 56 days. Liver retinoid stores were not affected by TCB treatment. These results clearly demonstrate that fish metabolize retinoic acid through a hydroxylation step which can be accelerated by a cytochrome P4501-inducing coplanar PCB. Given the pronounced biological activity of retinoic acid and closely related retinoids, increased retinoic acid metabolism could explain some of the effects of PCBs in fish.
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ISSN:0166-445X
1879-1514
DOI:10.1016/0166-445X(94)00091-4