The blood levels of hemoglobin(Hb), cerrulo-plasmin (Cp), superoxide dismutase (SOD), glu-tathion peroxidase (GSH-Px), malonaldehyde(MAD) and the concentrition of Cd, Fe, Cu andSe in liver were measured 4 weeks after weanedSprague-Dawley rats fed on Cd-supplemented diet(Cd 100mg/kg). The results indicated that. theconcentrition of Fe, Cu and Se in liver and theblood levels of Hb, SOD and GSH-Px activity weredecreased, but the blood level of MAD was in-creased by dietary Cd. The abnormal changes andanemia induced by Cd were able to be partially al-leviated by oral supplementing Fe, Cu and Se. Itsuggested. that Cd was able to produce peroxidationof erythrocyte membrane lipids. It is a possiblemechanism of the decreased survival of erythrocyteand hemolysis by Cd.

The bran of black rice contains 210～480 ppm iron, 50～70ppm zinc and 14.1% protein. In order to evaluate the bioavailability of bran iron, its relative biological availability (RBA) has been studied by means of the hemoglobin regeneration technique in anemic rats. All the rats were divided into five groups, the low-iron basal diet was supplemented with 23ppm Fe of ferrous sulfate in group A, 11.5% bran in group B, 11.5% bran plus 0.2% Vc in group C, 11.5% bran plus 2.3% cooked lean pork in group D and nothing in group E as the negative control The efficiencies of converting iron from the diet of group A, B, C, D into hemoglobin were 59%, 33%, 33% and 39% respectively and the relative biological availabilities were 100%, 56%, 56% and 66% respectively.

The causes of Cd-induced anemia and the preventive effect of Fe, Zn or Cu was studied. Day-old male chicken were randomly divided on body weight to 6 groups:A, Basal diet; B, Basal diet + Cd; C, Basal diet + Cd + Fe; D, Basal diet + Cd + Zn, E, Basal diet + Cd + Cu, F, Basal Diet + Cd + Fe + Zn + Cu. After 3 weeks feeding, the parameters to evaluate anemia of the chicken were observed.The results indicated: 1. Dietary Cd produced normocytic hypochro-mic anemia in chicken. Its causes were related to the abnormal size and decreased resistance of RBC and the deficiency of Fe and Cu in the chicken. 2. Dietary supplement of Fe and Cu was able to prevent Cd-induced anemia, but Zn had no effect. 3. Dietary Cd produced growth retardation in chicken and it could be prevented by supplementing Fe, Zn or Cu.

A biological study was made to estimate the influence of excess dietary zinc, in vivo, on iron and copper status and their antagonism. Chicks were randomly divided into four groups (n= 22 each) according to body weight and were fed on experimental diet with different amounts of zinc, iron and copper for 28 days. The results were as follows; 1. Excess dietary zinc (400ppm) caused retardation of growth rate in experimental chicks, hypochromic anemia, elevation of blood and tissues (liver, kidney) zinc levels and lowering iron, copper and ceruloplasmin content,and eryth-rocyte Cu-Zn-superoxide dismutase activity; 2. Copper alone supplemented up to 40ppm to the excess zinc diet was able to improve the growth rate, body copper status and Cu-Za-superoxide dismutase activity, but no effect on anemia and body iron status; 3. Iron and copper were supplemented up to 400ppm and 40ppm respectively to excess zinc diet at same time, all the parameters were similar to the chicks fed basal diet. These data suggested that supplement of iron and copper at proper proportion to excess zinc diet can prevent the adverse effects of excess zinc on chicks.