Studies of the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on mammalian hepatic delta-aminolevulinic acid synthetase.

The toxicity of 2,3,7,8-tetrachlorodibenzop-dioxin (TCDD), a contaminant formed during the manufacture of the herbicide 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) is well known (1-4). The widespread utilization of this compound has caused increased concern about the potential health hazards created by the presence of TCDD in the environment. The articles which accompany this account, indeed, attest to the highly toxic nature of TCDD in both laboratory animals and man. Interest in TCI)D as a potential porphyrogenic agent arose when porphyria cutanea tarda, a form of hepatic porphyria, occurred in industrial workers associated with the manufacture of 2,4,5-T (5). Hepatic porphyria is a syndrome characterized by a variety of symptoms including the overproduction and excretion of porphyrins, pigmentation of the skin, photosensitivity, and intestinal and neurological disorders. The disease is characterized biochemically by an increase in the activity of the mitochondrial enzyme