Retinoic acid hydroxylation in rainbow trout ( Oncorhynchus mykiss ) and the effect of a coplanar PCB, 3,3′,4,4′-tetrachlorobiphenyl
Identifieur interne : 001B28 ( Main/Merge ); précédent : 001B27; suivant : 001B29Retinoic acid hydroxylation in rainbow trout ( Oncorhynchus mykiss ) and the effect of a coplanar PCB, 3,3′,4,4′-tetrachlorobiphenyl
Auteurs : Nicolas L. Gilbert [Canada] ; Marie-Josée Cloutier [Canada] ; Philip A. Spear [Canada]Source :
- Aquatic Toxicology [ 0166-445X ] ; 1995.
Abstract
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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DOI: 10.1016/0166-445X(94)00091-4
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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.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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