Brain Iron in the Rat: Extremely Slow Turnover in Normal Rats May Explain Long-Lasting Effects of Early Iron Deficiency

Abstract

A brief period of iron deficiency in the young rat, from 15 to 28 days of age, was previously found to result in a depression of brain iron that persisted long after other biochemical effects of iron deficiency had been reversed. In this study, we investigated two possible reasons for this observation: 1. a change in blood-brain permeability to iron and 2. a slow turnover of iron compounds in the brain. Normal rats aged 5, 7, 11, 17, 21, 34, and 59 days were injected intraperitoneally with 59FeCl3, 100,000 cpm/g body weight. In general, the uptake of label by the brain was proportional to the developmental increase in brain iron at each age and indicated no permeability barrier to iron. The turnover of brain iron compounds was studied after a single injection of 100,000 cpm/g 59FeCl3 at either 15 or 35 days of age. In the group injected at 15 days of age, venesection and intramuscular injections of iron dextran decreased the specific activity of blood iron and liver non-heme iron to about 5% that of brain non-heme iron. These conditions reduced the magnitude of errors due to recycling of isotope and simplified the interpretation of results. The results showed virtually no loss of counts from the brain between 50 and 150 days of age. The specific activity of total brain non-heme iron and ferritin iron fell only slightly during this period, to a degree that could be attributed primarily to the developmental increase in brain iron. We conclude that the failure to reverse early iron depletion of the brain is due to an extremely slow rate of replacement of brain compounds.