Abstract
1. 1. Chronic treatment with 0.07% hexachlorobenzene produced a prolonged intermediate porphyric stage in rats very different from the symptomatic porphyria-like syndrome produced by higher doses and longer treatment. 2. 2. Administration of further porphyrinogenic agents to rats in the intermediate porphyric stage induced acute episodes biochemically very similar to the human acute porphyric attack. 3. 3. Few of the excess porphyrins excreted by the rats were of hepatic origin. Faecal porphyrins apparently were synthesized in the intestinal tract, whilst urinary porphyrins originated mainly in the kidney, even during the acute episode.
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