Dietary iron deficiency in the rat. I. Abnormalities in energy metabolism of the hepatic tissue.

Severe iron deficiency was induced in rats by rearing nursing dams and their offspring on a diet comprising all the requisite nutrients and trace metals except iron. The iron deficient 5-week-old rats exhibited a severe anemia and a drastic decrease in iron content of the hepatic tissue and of the mitochondrial fraction. Cytochromes c + c1 and b were moderately but significantly reduced. A large increase in liver concentration was observed in iron-deficient animals; whereas there was no modification in total lipid, cholesterol, phospholipid and fatty acid composition of the mitochondrial membrane. Mitochondria from iron-deficient rats presented a partial uncoupling of the oxidative phosphorylation process. This functional derangement was completely reversed by the presence of either bovine serum albumin or L-carnitine plus ATP. This behaviour suggested that endogenous long-chain fatty acids could be primarily involved in the onset of mitochondrial dysfunction. The hepatic energy state of the liver appeared dramatically decreased under the pathological condition of severe iron-deficiency anemia. The possibility of a direct link between the partial loss of coupled functions observed in isolated mitochondria and the heavy energy deficit detected in the liver is discussed.