• 1 January 1977
    • journal article
    • research article
    • Vol. 17  (4) , 631-637
Abstract
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 .mu.g/kg per wk, i.p.) for 5 wk. Urine prophyrin excretion remained unchanged in the non-responsive mice but was increased in the responsive group 2 wk following the 1st dose and continued to rise. Upon sacrifice, uroporphyrinogen decarboxylase activity was 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.