THE EFFECTS OF SODIUM CHROMATE AND CARBON-TETRACHLORIDE ON THE URINARY-EXCRETION AND TISSUE DISTRIBUTION OF CADMIUM IN CADMIUM-PRETREATED RATS
THE EFFECTS OF SODIUM CHROMATE AND CARBON-TETRACHLORIDE ON THE URINARY-EXCRETION AND TISSUE DISTRIBUTION OF CADMIUM IN CADMIUM-PRETREATED RATS
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DOI：
10.1016/0041-008x(81)90022-3
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发表时间：
1981-01-01
影响因子：
3.8
通讯作者：
LAUWERYS, RR
中科院分区：
文献类型：
--
作者：
BERNARD, AM;LAUWERYS, RR
通过口服或腹腔注射给大鼠施用无毒剂量的 Cd2+。路线。随后用 Na2CrO4（10 或 20 mg/kg，皮下注射）或 CCl4（0.5 或 1 ml/kg，胃内）处理。通过测定尿液中的总蛋白和氨基酸以及通过十二烷基硫酸钠-聚丙烯酰胺凝胶电泳分析尿蛋白来获得肾损伤的证据。通过测定山梨醇脱氢酶和谷氨酸丙酮酸转氨酶的血清活性来评估肝损伤。 CCl4 对 Cd2+ 的尿排泄和组织分布的影响因肝损伤是否与广泛的肾脏病变相关而异。当肾功能未发生或仅发生中度改变时，CCl4 诱导的肝损伤导致 Cd2+ 从肝脏转移至肾脏。这种转移的证据是肝脏中总 Cd2+ 和金属硫蛋白结合 Cd2+ 的减少以及肾脏中水平的增加。 Cd2+ 的尿排泄量略有增加。当CCl4引起的肝损伤伴有广泛的肾脏病变时，肝脏释放的Cd2+在肾脏中的积累减少，大量Cd2+通过尿液排出。将Na2CrO4给予Cd2+预处理的大鼠后，尿中Cd2+排泄量急剧且可逆地增加。这种增加与肾脏中储存的 Cd2+ 量和施用的 Na2CrO4 剂量成正比。 Cd2+ 经肾脏排泄到尿液中，其中总 Cd2+ 和金属硫蛋白结合的 Cd2+ 随 Na2CrO4 给药剂量的增加而减少。结果表明，有 2 种机制可能导致 Cd2+ 尿排泄增加；受损肾脏 (Na2CrO4) 直接将 Cd2+ 释放到尿液中，或者当大量 Cd2+ 从受损肝脏 (CCl4) 释放到血液中时，可证明肾小管对血浆循环 Cd2+ 的重吸收减少。结果支持这样的假设：慢性 Cd2+ 中毒导致的肾脏损伤可能导致肾脏中储存的 Cd2+ 损失增加。
Rats were administered nontoxic doses of Cd2+ by oral or i.p. routes. They were subsequently treated with either Na2CrO4 (10 or 20 mg/kg, s.c.) or CCl4 (0.5 or 1 ml/kg, intragastric). Evidence of renal damage was obtained from determination in urine of total protein and amino acids and from analysis of urinary proteins by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Liver damage was evaluated by determining serum activities of sorbitol dehydrogenase and glutamate pyruvate transaminase. Effects of CCl4 on urinary excretion and tissue distribution of Cd2+ varied depending on whether liver damage was associated with extensive renal lesions. When renal function was not or only moderately altered, induction of liver damage by CCl4 resulted in a transfer of Cd2+ from liver to kidney. This transfer was evidenced by decreased total Cd2+ and metallothionein-bound Cd2+ in liver and increased levels in kidney. Urinary excretion of Cd2+ was slightly increased. When liver damage induced by CCl4 was associated with extensive kidney lesions, accumulation of Cd2+ released from liver in kidney was reduced and large amounts of Cd2+ were excreted in urine. Administration of Na2CrO4 to Cd2+-pretreated rats gave rise to a sharp and reversible increase in urinary excretion of Cd2+. This increase was proportional to amount of Cd2+ stored in kidney and to dose of Na2CrO4 administered. Cd2+ excreted in urine originated from kidney in which total Cd2+ and metallothionein-bound Cd2+ were reduced in proportion to dose of Na2CrO4 administered. Results suggested 2 mechanisms that may lead to increased urinary excretion of Cd2+; a direct release of Cd2+ into urine from damaged kidney (Na2CrO4) or a decreased tubular reabsorption of plasma circulating Cd2+ evidenced when large amounts of Cd2+ were released into blood from damaged liver (CCl4). Results supported the hypothesis that kidney damage due to chronic Cd2+ poisoning may lead to increased loss of Cd2+ stored in kidney.