Jejunal biopsies were obtained from five iron-deficient infants 24 to 32 hours after an intramuscular injection of iron-dextran. Newly produced cells at the base of the villus appeared to have a higher cytochrome-oxidase activity compared to the older cells at the tip which were produced during a period of iron deficiency. These results in man, similar to those previously described in the rat, suggest that the repair of intestinal cytochrome-oxidase activity which accompanies treatment of iron deficiency is limited by the rate of new cell production.
In the iron-deficient rat histochemical evidence of cytochrome-oxidase repair corresponds closely to the extent of migration of new cells up the villus as indicated by autoradiography, between 8 and 48 hours following simultaneous administration of tritiated thymidine and iron-dextran. Colchicine, which arrests cell division at metaphase, interferes with cytochrome-oxidase repair when administered simultaneously with iron-dextran.
Enzymes not known to contain iron or require it as a cofactor were assayed in jejunal scrapings from iron-deficient and control rats. Aspartate transcarbamylase, alkaline phosphatase, sucrase, and maltase activities were normal in the intestinal mucosa of the iron-deficient rat.
No intestinal malfunction was demonstrated in the iron-deficient rat by determination of fecal fat excretion, I131 PVP excretion, and transport of glucose and galactose in everted sacs of the jejunum and the ileum.
Effect of Perinatal Brain Iron Deficiency on Cytochrome Oxidase Activity of Cognitive and Non-Cognitive Structures of the Brain Following a Hypoxic-Ischemic Injury in Neonatal Rats