ISOTOPIC STUDIES OF PORPHYRIN AND HEMOGLOBIN METABOLISM II. THE BIOSYNTHESIS OF COPROPORPHYRIN III IN EXPERIMENTAL LEAD POISONING* BY MOISfiS GRINSTEIN,?

It is now well established that glycine is a direct nitrogenous precursor of hemoglobin protoporphyrin in rats (l), rabbits (Z), dogs (3), and humans (4), of coproporphyrin I in dogs and humans (3, 5), of uroporphyrin I in humans (5), and of stercobilin in humans (5, 6). It is well known that lead intoxication in rabbits is associated with prompt and marked increases of urinary coproporphyrin III (7, 8). Three possibilities existed to explain these increases: (a) a derivation from destroyed hemoglobin (9), (b) new formation either in relation to a disturbed hemoglobin synthesis (10) or as an expression of some more obscure disturbance of pigment metabolism, (c) mobilization of free or bound coproporphyrin from tissue stores, with subsequent excretion in the urine. The administration of glycine labelled with N16 to lead-poisoned rabbits offered a means of deciding which of these three possibilities is actually represented. The present paper describes the results of such a study.