Bracken W M, Sharma R P
Toxicology. 1985 Mar 15;34(3):189-200. doi: 10.1016/0300-483x(85)90170-2.
In an effort to examine cellular responses to cadmium insult a bovine kidney cell line was used to monitor select cell functions for toxicity related alterations. Cadmium concentrations used ranged between 0.2 and 2.5 microM CdCl2 and elicited 0-85% cytotoxicity (cell attachment); 24-h incubations were used for all studies. Toxicity related inhibition of leucine incorporation into cellular protein and thymidine incorporation into DNA was noted. Decreases in protein synthesis activity closely paralleled the cytotoxicity profile; DNA synthesis was a less sensitive indicator to toxicity. K+-dependent phosphatase (KP), acid phosphatase (AP) and succinate dehydrogenase (SDH) were monitored in surviving cells and in a cell-free system. Significant inhibitions were detected for all enzyme activities following a 24 h culture with cadmium. KP and AP were most sensitive. In the cell-free system KP was significantly inhibited with 0.1 microM cadmium; AP and SDH were either unchanged or sensitive only at concentrations of 100 microM cadmium or greater. Reduced glutathione (GSH) concentration in surviving cells was elevated up to 7-fold over control cultures. The elevation occurred in a progressive toxicity-related manner.
为了研究细胞对镉损伤的反应，使用了一种牛肾细胞系来监测某些细胞功能，以了解与毒性相关的变化。所用镉浓度范围为0.2至2.5微摩尔氯化镉，引起了0 - 85%的细胞毒性（细胞附着）；所有研究均采用24小时孵育。观察到与毒性相关的亮氨酸掺入细胞蛋白质以及胸苷掺入DNA的抑制作用。蛋白质合成活性的降低与细胞毒性情况密切平行；DNA合成对毒性的敏感性较低。在存活细胞和无细胞体系中监测了钾离子依赖性磷酸酶（KP）、酸性磷酸酶（AP）和琥珀酸脱氢酶（SDH）。用镉培养24小时后，所有酶活性均检测到显著抑制。KP和AP最为敏感。在无细胞体系中，0.1微摩尔镉可显著抑制KP；AP和SDH要么没有变化，要么仅在100微摩尔或更高浓度的镉时才敏感。存活细胞中还原型谷胱甘肽（GSH）浓度比对照培养物升高了7倍。这种升高以与毒性相关的渐进方式发生。
