Bracken W M, Sharma R P, Kleinschuster S J
Toxicology. 1984 Nov;33(2):93-102. doi: 10.1016/0300-483x(84)90065-9.
A bovine kidney cell culture system was used to assess what relationship cadmium (Cd) uptake and subcellular distribution had to cadmium chloride induced cytotoxicity. Twenty-four hour incubation with 0.1-10 microM Cd elicited 0-90% cytotoxicity. Fifty percent cytotoxicity was estimated to result from 0.8 microM Cd. A concentration-related Cd accumulation paralleled the cytotoxicity profile. The time-course for Cd accumulation was linear for the first 6 h of exposure and plateaued by 18 h post-exposure. When the degree of cytotoxicity was compared with the cellular Cd burden at 24 h post-treatment a least-squares linear regression analysis (r = 0.93) indicated a direct relationship. Subcellular distribution studies indicated greater than 90% Cd recovery from the soluble supernatant (105 000 g) at all levels of cytotoxicity studied. Metallothionein sequestered less than 25% of the cellular Cd. As a result of the correlation of the degree of cytotoxicity with the cellular Cd burden and the independence of subcellular distribution from cytotoxicity, a cumulative mechanism of toxicity for Cd in MDBK cells was suggested.
采用牛肾细胞培养系统来评估镉（Cd）的摄取和亚细胞分布与氯化镉诱导的细胞毒性之间的关系。用0.1 - 10微摩尔/升的镉孵育24小时会引发0 - 90%的细胞毒性。估计50%的细胞毒性是由0.8微摩尔/升的镉引起的。与浓度相关的镉积累与细胞毒性曲线平行。镉积累的时间进程在暴露的前6小时呈线性，在暴露后18小时达到平稳状态。当将细胞毒性程度与处理后24小时的细胞镉负荷进行比较时，最小二乘线性回归分析（r = 0.93）表明存在直接关系。亚细胞分布研究表明，在所研究的所有细胞毒性水平下，从可溶性上清液（105000克）中回收的镉超过90%。金属硫蛋白螯合的细胞镉不到25%。由于细胞毒性程度与细胞镉负荷之间的相关性以及亚细胞分布与细胞毒性的独立性，提示了镉在MDBK细胞中的累积毒性机制。
