Abstract
The daily administration of large doses of m-dichlorobenzene (m-DCB) causes experimental hepatic porphyria in rats by induction of δ-aminolevulinic acid synthetase (ALA synthetase). However, smaller doses of m-DCB produce a biphasic stimulation of both urinary coproporphyrin excretion and liver ALA synthetase. The decline of ALA synthetase and urinary coproporphyrin despite continued daily dosage is associated with an increase in activity of the liver drug-metabolizing systems and decreasing serum m-DCB levels. The most probable explanation for the self-limiting action of m-DCB is stimulation by the drug of its own metabolism.
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