Department of Poultry Science, NC State University, Box 7608, 27695-7608, Raleigh, NC.
Biol Trace Elem Res. 1987 Dec;14(3):225-35. doi: 10.1007/BF02795689.
The interaction of dietary iron levels on vanadium toxicity was studied in chicks. Dietary iron levels ranged from a deficiency, ca. 10 ppm, to an adequacy, 100 ppm supplemental iron. to an excess, 1000 ppm supplemental iron. Vanadium was fed at 10, 20, and 40 ppm. Vanadium toxicity as measured by chick growth was more severe in the iron-deficient animals than in those receiving supplemental iron. The increase in degree of toxicity in the iron-deficient animals was accompanied by an increase in the liver vanadium, both total and concentration. The addition, of vanadium to the diet did not influence the iron concentration of the liver or kidney. Radioisotope, studies with(48)V revealed that the absorption of vanadium was not influenced by the iron concentration of the diet, but that the iron-deficient animals retained more vanadium in the blood and liver and less in the bone than did the iron supplemented animals. It is proposed that the degree of iron saturation of transferrin and ferritin to which vanadium can bind is a possible explanation for the results obtained.
研究了膳食铁水平对钒毒性的相互作用。膳食铁水平从缺乏(约 10ppm)到充足(补充 100ppm 铁)到过量(补充 1000ppm 铁)不等。钒的添加量为 10、20 和 40ppm。用雏鸡生长来衡量,钒毒性在缺铁动物中比在补充铁的动物中更为严重。在缺铁动物中,毒性程度的增加伴随着肝钒含量的增加,包括总量和浓度。向饮食中添加钒不会影响肝脏或肾脏的铁浓度。用(48)V 进行的放射性同位素研究表明,钒的吸收不受饮食中铁浓度的影响,但缺铁动物在血液和肝脏中保留的钒比补充铁的动物多,而在骨骼中保留的钒比补充铁的动物少。据推测,转铁蛋白和铁蛋白中铁饱和度的程度可能是解释所获得结果的原因。