Klimczak J, Wiśniewska-Knypl J M, Kolakowski J
Toxicology. 1984 Sep 14;32(3):267-76. doi: 10.1016/0300-483x(84)90079-9.
Exposure of rats to 0.1 and 0.5 mg Cd/kg subcutaneously (s.c.) thrice weekly for 5 weeks resulted in an accumulation of cadmium in the liver in concentrations of 40 and 95 micrograms/g tissue, respectively, and a microsomal burden of Cd amounting to approx. 2-3% of the retained cadmium. The cytoplasm contained about 80% of the cadmium. At an exposure dose of 0.1 mg Cd/kg, stimulation of lipid peroxidation by 22% and inhibition of ALA synthetase by 16% in the liver were observed. The higher exposure of 0.5 mg Cd/kg caused an inhibition of microsomal monooxygenase with depression of cytochrome P-450 and cytochrome b5 by 20% (over 2-fold prolongation of hexobarbital sleeping time and statistically significant decrease of activity of aniline p-hydroxylase). The loss of cytochrome P-450 probably was due to an intensified lipid peroxidation and induction of heme oxygenase (30% and 60% over control, respectively). Sequestration of cadmium by cytoplasm (metallothionein) does not protect microsomes against cadmium accumulation and specific biochemical disturbances.
每周三次皮下注射（s.c.）0.1毫克/千克和0.5毫克/千克的镉，持续5周，结果大鼠肝脏中镉的蓄积浓度分别为40微克/克组织和95微克/克组织，镉的微粒体负荷约占留存镉的2%-3%。细胞质中含有约80%的镉。在暴露剂量为0.1毫克/千克时，观察到肝脏中脂质过氧化作用增强22%，δ-氨基-γ-酮戊酸（ALA）合成酶受到16%的抑制。较高的0.5毫克/千克暴露剂量导致微粒体单加氧酶受到抑制，细胞色素P-450和细胞色素b5降低20%（己巴比妥睡眠时间延长超过2倍，苯胺对羟基化酶活性有统计学意义的下降）。细胞色素P-450的损失可能是由于脂质过氧化作用增强和血红素加氧酶的诱导（分别比对照高30%和60%）。细胞质（金属硫蛋白）对镉的螯合并不能保护微粒体免受镉的蓄积和特定生化干扰。
