Porphyrin Metabolism in Experimental Hepatic Siderosis in the Rat

Abstract

S ummary . Experimental hepatic siderosis in the rat due to dietary iron overload produced increased urinary excretion of uro‐ and coproporphyrin which was further aggravated by concurrent drinking of alcohol. On the basis of these findings it is considered very likely that the invariable presence of hepatic siderosis in symptomatic porphyria is more than incidental and that the presence of excessive iron in the liver cells is an important factor determining the development of symptomatic porphryia. Liver ALA synthetase activity was increased in the alcohol‐consuming animals but iron overload alone had no effect on the activity of this enzyme. The mechanism whereby siderosis influences hepatic porphyrin metabolism is unknown. No effect on hepatic mitochondrial coproporphyrinogen oxidase was found. It is suggested that in the siderotic animals and in patients with symptomatic porphyria there is interference with a normal disposal route for excessive haem precursors.