Effects of iron-loading and ethanol treatment on rat porphyrin metabolism

Rats were fed for 50 weeks with a standard diet containing 5.9% ferric ammonium sulphate. Half of these animals drank normal water, and the other half water containing 5% ethanol (groups 1 and 2). Two other groups received normal food, but drank water containing 5 or 10% ethanol (groups 3 and 4) for 40 weeks. Histologic examinations revealed that the iron-loading resulted in only mild hepatic siderosis in groups 1 and 2, the degree of siderosis not differing appreciably in the two groups. The ethanol led to fatty degeneration too in the liver of animals in group 2. Both iron-loading and ethanol treatment, either separately or in combination, increased the porphyrin excretion, but the distribution of the various porphyrins in the urine and faeces showed merely the symptoms of an aspecific poisoning. A significantly elevated uroporphyrin excretion was not observed in any of the groups, and thus the results support the view that dietary iron-loading and ethanol consumption can not be regarded as direct aetiologic factors in the pathomechanism of porphyria cutanea tarda. At the same time, the results suggest that vitamin E therapy, frequently employed effectively in porphyria cutanea tarda, can not be considered a causal intervention as regards the mechanism of action.