Differential Susceptibility of Germ and Leydig Cells to Cadmium-Mediated Toxicity: Impact on Testis Structure, Adiponectin Levels, and Steroidogenesis.
Differential Susceptibility of Germ and Leydig Cells to Cadmium-Mediated Toxicity: Impact on Testis Structure, Adiponectin Levels, and Steroidogenesis.
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DOI：
10.1155/2017/3405089
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发表时间：
2017
影响因子：
--
通讯作者：
Matta SLP
中科院分区：
文献类型：
--
作者：
Cupertino MC;Novaes RD;Santos EC;Neves AC;Silva E;Oliveira JA;Matta SLP
本研究探讨了镉急性毒性中生殖细胞和间质细胞死亡、睾酮和脂联素水平之间的关系。将氯化镉以单剂量给予五组大鼠：G1（0.9%NaCl）和G2至G5（0.67、0.74、0.86和1.1 mg Cd/kg）。7天后，将动物安乐死，并分析睾酮和睾丸。剂量依赖性镉在睾丸中的积累被确定。在0.86和1.1 mg/kg剂量下，动物表现出明显的炎症浸润和生精上皮组织解体。虽然Leydig细胞形态学上对Cd毒性具有抗性，但观察到大量生殖细胞死亡和DNA氧化和断裂。虽然数量密度的睾丸间质细胞是不变的，睾酮水平显着受损的动物暴露于0.86和1.1毫克镉/公斤，发生在平行的减少总脂联素和高分子量脂联素水平的增加。我们的研究结果表明，睾丸间质细胞和生殖细胞表现出不同的微观结构对镉毒性的抗性。虽然生殖细胞是镉诱导毒性的主要目标，但即使暴露于高剂量的镉，间质细胞仍能抵抗死亡。尽管形态阻力，类固醇激素的严重受损镉暴露，脂联素生产的不平衡可能有关的事件。
This study investigated the relationship between germ and Leydig cell death, testosterone, and adiponectin levels in cadmium-mediated acute toxicity. Cadmium chloride was administered in a single dose to five groups of rats: G1 (0.9% NaCl) and G2 to G5 (0.67, 0.74, 0.86, and 1.1 mg Cd/kg). After 7 days, the animals were euthanized, and the testosterone and testes were analyzed. Dose-dependent Cd accumulation in the testes was identified. At 0.86 and 1.1 mg/kg, animals exhibited marked inflammatory infiltrate and disorganization of the seminiferous epithelium. While Leydig cells were morphologically resistant to Cd toxicity, massive germ cell death and DNA oxidation and fragmentation were observed. Although numerical density of Leydig cells was unchanged, testosterone levels were significantly impaired in animals exposed to 0.86 and 1.1 mg Cd/kg, occurring in parallel with the reduction in total adiponectins and the increase in high-molecular weight adiponectin levels. Our findings indicated that Leydig and germ cells exhibit differential microstructural resistance to Cd toxicity. While germ cells are a primary target of Cd-induced toxicity, Leydig cells remain resistant to death even when exposed to high doses of Cd. Despite morphological resistance, steroidogenesis was drastically impaired by Cd exposure, an event potentially related to the imbalance in adiponectin production.
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