Association between induction of aryl hydrocarbon hydroxylase and depression of uroporphyrinogen decarboxylase activity.
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Mice that were genetically responsive (C57BL/6J) or non-responsive (DBA/2J) to induction of aryl hydrocarbon hydroxylase were treated with equal doses of 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (25 microgram/kg/wk, i.p.) for five weeks. Urine porphyrin excretion remained unchanged in the non-responsive mice but was increased in the responsive group two weeks following the first dose and continued to rise. Upon sacrifice, uroporphyrinogen decarboxylase activity was found to be normal in the non-responsives but decreased 48% in the responsive mice. These results suggest a relationship between induction of aryl hydrocarbon hydroxylase and the decreased uroporphyrinogen decarboxylase activity resulting from exposure to chlorinated aromatic hydrocarbons.
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