Nordberg G F, Goyer R, Nordberg M
Arch Pathol. 1975 Apr;99(4):192-7.
Cadmium-induced metallothionein may have a paradoxical role in the pathogenesis of cadmium toxicity. Mice are protected from cadmium-induced testicular necrosis by metallothionein, but in this experiment it was shown that cadmium-metallothionein complex injected into mice results in higher cadmium levels in renal cortex and more severe renal tubular cell injury than a comparable dose of cadmium chloride administered by the same route. Also, an injection of 1.1 mg/kg of body weight or more of cadmium bound to metallothionein was fatal to male CGA mice within seven days whereas five times this dose of cadmium administered as cadmium chloride was needed to produce a similar effect. A reason for the difference in renal effects of these two forms of cadmium has not been determined but may be related to differences in absorption or transport by renal tubular lining cells.
镉诱导的金属硫蛋白在镉毒性的发病机制中可能具有矛盾的作用。金属硫蛋白可保护小鼠免受镉诱导的睾丸坏死,但在本实验中发现,通过相同途径向小鼠注射镉-金属硫蛋白复合物,与注射同等剂量的氯化镉相比,会导致肾皮质中镉水平更高,肾小管细胞损伤更严重。此外,向雄性CGA小鼠注射1.1毫克/千克体重或更多与金属硫蛋白结合的镉,会在7天内导致小鼠死亡,而通过氯化镉形式给予该剂量5倍的镉才会产生类似效果。这两种形式的镉对肾脏影响不同的原因尚未明确,但可能与肾小管衬里细胞的吸收或转运差异有关。