PubMed1983
Tissue ferritin metabolism was compared in control and ascorbic acid (AA) deficient guinea-pigs. Concentrations of ferritin protein in the liver (0.98 +/- 0.61 mg/g wet weight) and spleen (0.48 +/- 0.23 mg/g) of control animals did not change after tissue depletion of AA. Iron dextran (75 mg/kg weight, i.m.) caused a 4-5-fold increase in tissue ferritin concentrations in controls whereas no increase in tissue ferritin occurred in scorbutic animals. The rise in tissue total iron concentration was similar in the two groups. Liver ferritin synthesis was similar in control and scorbutic animals. After stimulation with iron (8 mg/kg iron dextran i.v.), ferritin synthesis rose in both groups of animals. However, the pattern of response differed. At 24 h after iron dextran, ferritin synthesis in controls was still significantly elevated (P less than 0.001) and liver ferritin protein continued to rise, whereas in scorbutic animals, ferritin synthesis had declined to pre-iron injection levels, and no rise in ferritin protein values occurred. It is concluded that the ferritin synthetic apparatus in AA deficient tissues remained intact and capable of responding to added iron. The absence of a sustained elevation in tissue ferritin protein after an iron load appeared to be due to inadequate stimulation of ferritin synthesis by intracellular iron. It is suggested that AA has a physiological role in the reduction of intracellular iron and that it is the reduced form of iron which stimulates ferritin synthesis. Abnormalities of iron metabolism occur in AA depleted tissues when the quantity of Fe3+ entering cells exceeds the residual reducing capacity of those cells.