Continued depression of hepatic uroporphyrinogen decarboxylase activity caused by hexachlorobenzene or 2,3,7,8-tetrachlorodibenzo-p-dioxin despite regeneration after partial hepatectomy.
Hepatic uroporphyrinogen decarboxylase activity in male C57BL/10 mice was maintained in regenerated liver after recovery from two-thirds hepatectomy. In contrast, there was little increase in enzyme activity in regenerated liver from animals previously treated with hexachlorobenzene (HCB) or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). These chemicals initially cause depression of uroporphyrinogen decarboxylase activity over a time much longer than the period allowed for regeneration. Estimation of HCB levels showed that there was only a small amount of redistribution to the liver during regrowth. The results demonstrate that HCB and TCDD induce either formation of a toxic metabolite or some other inhibitory process and that this can be sustained for a long period which delays recovery to the normal state.
D000818:Animals; D002262:Carboxy-Lyases / Q000037:antagonists & inhibitors*; D002722:Chlorobenzenes / Q000633:toxicity*; D004147:Dioxins / Q000633:toxicity*; D006498:Hepatectomy; D006581:Hexachlorobenzene / Q000633:toxicity*; D008099:Liver / Q000201:enzymology*; D008115:Liver Regeneration; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D000072317:Polychlorinated Dibenzodioxins / Q000633:toxicity*; D014575:Uroporphyrinogen Decarboxylase / Q000037:antagonists & inhibitors*
D002722:Chlorobenzenes; D004147:Dioxins; D000072317:Polychlorinated Dibenzodioxins; D006581:Hexachlorobenzene; D002262:Carboxy-Lyases; D014575:Uroporphyrinogen Decarboxylase