King L M, Anderson M B, Sikka S C, George W J
ARS USDA, Germplasm and Gamete Physiology Laboratory, Beltsville, MD 20705, USA.
Arch Toxicol. 1998 Oct;72(10):650-5. doi: 10.1007/s002040050556.
The role of strain differences in cadmium tissue distribution was studied using sensitive (129/J) and resistant (A/J) mice. These murine strains have previously been shown to differ in their susceptibility to cadmium-induced testicular toxicity. Cadmium concentration was measured in testis, epididymis, seminal vesicle, liver, and kidney at 24 h after cadmium chloride exposure (4, 10, and 20 micromol/kg CdCl2). The 129/J mice exhibited a significant increase in cadmium concentration in testis, epididymis, and seminal vesicle at all cadmium doses used, compared to A/J mice. However, cadmium concentrations in liver and kidney were not different between the strains, at any dose, indicating that cadmium uptake is similar in these organs at 24 h. These murine strains demonstrate similar hepatic and renal cadmium uptake but significantly different cadmium accumulation in the reproductive organs at 24 h. The mechanism of the protective effect of zinc on cadmium toxicity was studied by assessing the impact of zinc acetate (ZnAc) treatment on cadmium concentrations in 129/J mice after 24 h. Zinc pretreatment (250 micromol/kg ZnAc), given 24 h prior to 20 micromol/kg CdCl2 administration, significantly decreased the amount of cadmium in the testis, epididymis, and seminal vesicle of 129/J mice, and significantly increased the cadmium content of the liver after 24 h. Cadmium levels in the kidney were unaffected at this time. Zinc pretreatment also prevented the cadmium-induced decrease in testicular sperm concentration and epididymal sperm motility seen in 129/J mice. These findings suggest that the differences in the two murine strains may be attributed partly to the differential accumulation of cadmium in murine gonads. This may be caused by strain differences in the specificity of cadmium transport mechanisms. The protective role of zinc in cadmium-induced testicular toxicity in the sensitive strain may be due to an interference in the cadmium uptake by susceptible reproductive organs.
利用敏感型（129/J）和抗性型（A/J）小鼠研究了品系差异在镉组织分布中的作用。此前已表明，这些小鼠品系对镉诱导的睾丸毒性的易感性存在差异。在氯化镉暴露（4、10和20微摩尔/千克CdCl₂）24小时后，测量睾丸、附睾、精囊、肝脏和肾脏中的镉浓度。与A/J小鼠相比，在所有使用的镉剂量下，129/J小鼠睾丸、附睾和精囊中镉浓度均显著增加。然而，在任何剂量下，两个品系肝脏和肾脏中的镉浓度并无差异，这表明在24小时时这些器官对镉的摄取相似。这些小鼠品系在24小时时表现出相似的肝脏和肾脏镉摄取，但生殖器官中的镉积累存在显著差异。通过评估醋酸锌（ZnAc）处理对24小时后129/J小鼠镉浓度的影响，研究了锌对镉毒性的保护作用机制。在给予20微摩尔/千克CdCl₂前24小时进行锌预处理（250微摩尔/千克ZnAc），显著降低了129/J小鼠睾丸、附睾和精囊中镉的含量，并在24小时后显著增加了肝脏中的镉含量。此时肾脏中的镉水平未受影响。锌预处理还预防了129/J小鼠中镉诱导的睾丸精子浓度降低和附睾精子活力下降。这些发现表明，这两个小鼠品系的差异可能部分归因于镉在小鼠性腺中的差异积累。这可能是由于镉转运机制特异性的品系差异所致。锌在敏感品系中对镉诱导的睾丸毒性的保护作用可能是由于干扰了易感生殖器官对镉的摄取。
