Iron status in rats fed on diets containing marginal amounts of vitamin A.

Severe vitamin A deficiency in rats is known to cause anaemia associated with growth retardation and impaired water retention. However, study of the effect of marginal vitamin A intake is of more interest because such intake may mirror the situation in humans in many developing countries. Therefore, in two experiments, the effect of marginal vitamin A deficiency on Fe status was investigated in male rats. After 28 d of feeding either low- or high-vitamin A diets (0 or 120 v. 1200 retinol equivalents/kg feed), body weight and feed intake were not influenced by the level of vitamin A in the diet. Liver weight was lowered by vitamin A deficiency. Water intake was not influenced in rats fed on a low-vitamin A diet. Plasma retinol concentrations were decreased in rats fed on diets low in vitamin A. Marginal vitamin A deficiency produced slightly lower blood haemoglobin concentrations; it did not systematically affect packed cell volume. The concentration of Fe in liver was significantly higher when diets low in vitamin A were fed, but hepatic Fe mass was not affected. Significantly lower Fe levels were observed in femurs of rats with vitamin A deficiency. The effects on liver and femur Fe concentrations were seen with diets adequate in Fe but not with diets deficient in Fe. The efficiency of apparent Fe absorption was significantly increased by low intakes of vitamin A, provided that the dietary Fe concentration was adequate. It is speculated that depressed uptake of Fe by bone marrow is the primary feature of altered Fe status in rats with marginal vitamin A deficiency.

Iron and zinc status in rats with diet-induced marginal deficiency of vitamin A and/or copper.

The hypothesis was tested that there are interactions of marginal copper and vitamin A deficiency regarding iron and zinc status. Copper restriction (1 vs 5 mg Cu/kg diet) significantly lowered copper concentrations in plasma and tissues of rats and reduced blood hemoglobin, hematocrit, and iron concentrations in tibia and femur, but raised iron concentrations in liver. Vitamin A restriction (0 vs 4000 IU vitamin A/kg diet) reduced plasma retinol concentrations and induced a fall of blood hemoglobin and hematocrit. Neither copper nor vitamin A restriction for up to 42 d affected feed intake and body wt gain. There were no interrelated effects of vitamin A and copper deficiency on iron status. Copper deficiency slightly depressed liver, spleen, and kidney zinc concentrations. Vitamin A deficiency lowered zinc concentrations in heart, but only when the diets were deficient in copper.

Iron status in rats fed a purified diet without vitamin A.

The effect of vitamin A deficiency on iron status was investigated in rats. After 28 d of feeding either low or high vitamin A diets (0 vs 4000 IU of vitamin A per kg feed), the final body weight was slightly but significantly lowered by the low vitamin A diet. Plasma retinol concentrations were decreased in rats fed diets low in vitamin A. Marginal vitamin A deficiency produced slightly, but significantly lower blood hemoglobin concentrations; it did not clearly affect hematocrit. The concentration of iron in liver was significantly higher when diets low in vitamin A were fed while significantly lower levels were observed in femur.