This review discusses the absorption, storage, biotransformation, and excretion of chlorinated hydrocarbon insecticides; thus, it emphasizes those aspects of physiology that can be studied by the methods of analytical or ganic chemistry. The broader aspects of toxicity, as they relate to the me tabolism of these materials, were discussed by Winteringham & Barnes (1).This review emphasizes mammalian metabolism of the compounds, but con tains some information on their metaboli sm by other organisms, a subject that has already been reviewed by Perry (2). In relation to mammals, great est interest centers in numerous repeated doses that produce no obvious in jury and that are so small that they might be encountered under practical conditions in the use of insecticides. For this reason, DDT and related re sidual insecticides are emphasized, but some information is given on the chlorinated hydrocarbon fumigants.
The influence of diethylstilbestrol (DES) and testosterone propionate (TP) on the storage of DDT and its metabolite, DDE, was studied in normal and in gonadectomized rats. As expected, TP dosage increased the growth of female rats while DES administration inhibited the growth of males. Both hormones inhibited gonadal growth. Rats that received either DDT or hormone showed an increased liver weight/body weight ratio as compared to control animals. This effect was more marked in males than in females. DES increased DDT and DDE storage in fat in the male while TP decreased these values in the female. Similar effects of hormone dosage were noted on the ratio of DDE to total DDT-derived material stored in fat.
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