Dietary iron deficiency in the rat. II. Recovery from energy metabolism derangement of the hepatic tissue by iron therapy.

Severe iron deficiency in rats was found to be associated with abnormal lipid accumulation in the liver and impairment of the oxidative metabolism in the hepatic tissue. Iron therapy, consisting in oral administration to iron-deficient 4-week-old rats of iron succinyl-albumin complex, at a daily dose of 10 mg/kg body weight, over a period of 7 days, almost completely corrected these functional anomalies. This treatment fully reverted severe anemia associated with iron deficiency. The level of iron in the hepatic tissue and in the mitochondrial fraction also increased largely. By contrast, no significant improvement in the lowered level of cytochromes occurred. Iron supplements significantly decreased the abnormal level of liver total lipids and serum triglycerides. Concomitantly, iron repletion fully reverted the partial loss of coupled function in isolated mitochondria and the energy state perturbation of the liver. A close relationship among abnormal lipid accumulation, impairment of mitochondrial oxidative phosphorylation and energy derangement in the hepatic cell in this experimental model of severe dietary iron deficiency anemia appears to be likely.