Roberts S A, Schnell R C
Fundam Appl Toxicol. 1981 May-Jun;1(3):286-9. doi: 10.1016/s0272-0590(81)80130-3.
Cadmium, in dose of 0.84 mg/kg (ip), produces a marked inhibition in hepatic oxidative xenobiotic metabolism which results from a decreased cytochrome P-450 content in the male rat. The inhibitions in microsomal metabolism of aniline, ethylmorphine, or p-nitroanisole were not elicited by the 0.84 mg/kg cadmium dose in rats which had been pretreated (72 hours prior) with a lower dose of cadmium (0.21 mg Cd/kg, ip). Likewise, the decreases in both microsomal cytochrome P-450 content and in microsomal spectral binding of hexobarbital or aniline produced by the 0.84 mg/kg cadmium dose were not elicited in the rats pretreated with the low cadmium dose. The 0.21 mg/kg cadmium dose produced an increase (370%) in the cadmium-binding capacity as well as an increase (395%) in total hepatic metallothionein. These data are consistent with the hypothesis that the pretreatment of animals with relatively low cadmium doses produces an increase in the cellular levels of metallothionein which can then bind and ameliorate the toxicological effects of a subsequently administered toxic dose of cadmium.
腹腔注射剂量为0.84毫克/千克的镉，会使雄性大鼠肝脏的外源性物质氧化代谢显著受到抑制，这是由于细胞色素P - 450含量降低所致。在预先（72小时前）经较低剂量镉（腹腔注射0.21毫克镉/千克）处理的大鼠中，0.84毫克/千克的镉剂量并未引发对苯胺、乙基吗啡或对硝基苯甲醚微粒体代谢的抑制作用。同样，0.84毫克/千克的镉剂量所导致的微粒体细胞色素P - 450含量以及微粒体中己巴比妥或苯胺光谱结合的降低，在预先经低剂量镉处理的大鼠中也未出现。0.21毫克/千克的镉剂量使镉结合能力增加了370%，同时肝脏中总金属硫蛋白增加了395%。这些数据与以下假设一致：用相对低剂量的镉对动物进行预处理会使金属硫蛋白的细胞水平升高，进而能够结合并减轻随后给予的毒性剂量镉的毒理学效应。
