Interactions of chlorinated hydrocarbons with steroid hormones

Effects of chlorinated hydrocarbons of the DDT class in mammals were examined. Two effects were considered: a) induction of hepatic mixed function oxidase (MFO), and b) estrogenic activities. The induction of MFO was discussed primarily with reference to the enhancement of steroid hydroxylation. In turn, the increase in steroid hydroxylation by chlorinated hydrocarbons was usually accompanied by a decrease in the biological activity of endogenous and administered steroid hormones. The estrogenic activity of chlorinated hydrocarbons was found to reside primarily in the o,p'-DDT (a major contaminant of technical grade DDT). The mechanism of the estrogenic activity by DDT homologs was explored. It appears that o,p'-DDT acts like estradiol (E2). Similarly to E2, o,p'-DDT binds to the uterine cytosolic receptor. Furthermore, like E2, o,p'-DDT is a potent inducer of certain uterine enzymes. For instance induction of ornithine decarboxylase of about 200-fold was observed with a high dose (250 mg/kg body wt); however as little as 5 mg/kg of o,p'-DDT exhibited marked induction of this enzyme--about threefold. The above activities of the chlorinated hydrocarbons were considered with respect to the potential long-term toxic effects which these compounds might elicit.