Tewari P C, Kachru D N, Tandon S K
Environ Res. 1986 Oct;41(1):53-60. doi: 10.1016/s0013-9351(86)80167-0.
Male albino rats maintained on low-protein (9%) diets were dosed intraperitoneally with 0.75 mg Cd/kg, as cadmium chloride, for 20 days. Groups of these animals were provided with diets supplemented with 40 ppm Cu, 400 ppm Fe or a combination of both during the exposure period. Hepatic and renal distribution of Cd, Zn, Cu, and Fe along with activity of acid and alkaline phosphatases and ribonuclease and glutathione content were studied. Uptake of Cd both in liver and in kidney was significant and was accompanied by increased Zn and depletion of Fe concentration. The Cu level remained unaltered. Dietary supplementation of Cu or Fe interacted effectively and influenced the metal distribution. Acid and alkaline phosphatases in both liver and kidney were inhibited by Cd exposure. However, Cu and/or Fe supplements could to a varying degree offset the Cd-induced inhibition. Cadmium exposure did not, however, elicit any effect on hepatic and renal ribonuclease activity of low-protein-fed animals. The glutathione concentration registered profound increase on Cd exposure, possibly to act as a defence mechanism.
将雄性白化病大鼠饲养在低蛋白（9%）饮食中，以氯化镉的形式腹腔注射0.75毫克镉/千克，持续20天。在暴露期间，给这些动物分组提供补充了40 ppm铜、400 ppm铁或两者组合的饮食。研究了镉、锌、铜和铁在肝脏和肾脏中的分布，以及酸性和碱性磷酸酶、核糖核酸酶的活性和谷胱甘肽含量。镉在肝脏和肾脏中的摄取量显著，同时伴随着锌含量的增加和铁浓度的降低。铜水平保持不变。饮食中补充铜或铁产生了有效的相互作用，并影响了金属分布。镉暴露抑制了肝脏和肾脏中的酸性和碱性磷酸酶。然而，铜和/或铁补充剂可以在不同程度上抵消镉诱导的抑制作用。然而，镉暴露对低蛋白喂养动物的肝脏和肾脏核糖核酸酶活性没有产生任何影响。镉暴露后谷胱甘肽浓度显著增加，可能起到防御机制的作用。
