Chronic alcohol consumption in rats leads to a decrease in uroporphyrinogen decarboxylase activity in liver and spleen, associated with a pathologic porphyrinuria. The toxic effect of alcohol on the biochemical pathogenesis of chronic hepatic porphyria was studied. Results confirmed the transition of symptomatic coproporphyrinuria to chronic hepatic porphyria as observed in man and the progression of biochemical phases of chronic hepatic porphyria into the clinical phase, i.e., the development from latent to manifest stages under chronic alcohol ingestion.