Lyall V, Chauhan V P, Prasad R, Sarkar A K, Nath R
Toxicol Lett. 1982 Jul;12(2-3):131-5. doi: 10.1016/0378-4274(82)90175-8.
In rats chronically treated with varying doses of cadmium (Cd) (0.25, 0.50, 0.75 and 1.0 mg/kg body wt.), i.p., every alternate day for 7 weeks, a decrease in the ascorbic acid (AA) content of adrenals and liver was observed. In the adrenals AA depletion was significant and dose-dependent at all concentrations. In liver the decrease was significant only at a concentration of 0.75 and 1.00 mg/kg but the spleen did not show any change in AA content. Urinary excretion of beta2-microglobulin with increasing doses of Cd indicated progressive renal tubular damage. The decrease in tissue AA status was correlated with the severity of the renal tubular damage resulting in an inhibition of its reabsorption from the kidneys.
给大鼠腹腔注射不同剂量的镉（Cd）（0.25、0.50、0.75和1.0毫克/千克体重），每隔一天注射一次，持续7周，结果观察到肾上腺和肝脏中抗坏血酸（AA）含量下降。在肾上腺中，所有浓度下AA的耗竭都很显著且呈剂量依赖性。在肝脏中，只有在浓度为0.75和1.00毫克/千克时下降才显著，但脾脏的AA含量没有变化。随着镉剂量增加，β2-微球蛋白的尿排泄表明肾小管损伤逐渐加重。组织中AA状态的下降与肾小管损伤的严重程度相关，导致其从肾脏的重吸收受到抑制。
