Chronic copper exposure impaired spermatogenesis in adult male mice. The aim of this study was to determine whether chronic copper exposure can induce apoptosis of testicular cell and hypospermatogenesis via disturbing testosterone synthesis in adult male mice. In the present study, sixty CD-1 male mice were randomly divided into four groups, and were continuously administered for 8 weeks by oral gavage with copper sulfate at a dose of 0, 25, 100, and 150 mg/kg/day, respectively. We determined the content of serum and testicular copper, testicular coefficient, testicular histopathology, sperm count and motility, the mRNA and protein levels of Caspase-3, Bax, and Bcl-2, Leydig cell count, testosterone content, testosterone synthetase, and testosterone synthesis-related genes. The results showed that the copper levels in serum increased in a dose-dependent manner, and the copper levels in testes were significantly related to serum copper levels. Male mice given copper sulfate 100 and 150 dosage groups showed significant decreased in sperm motility and sperm number as well as increased in testes damage, and there was no significant change in testicular coefficient in the four groups. The mRNA levels of Bcl-2 decreased and Caspase-3 increased in 150 dosage group, and Bax increased in two higher dosage groups. Meanwhile, Caspase-3 and Bax proteins increased in 150 dosage group, and Bcl-2 protein decreased in three copper treatment groups. Nevertheless, there were no differences on the levels of testosterone content and testosterone synthetase of 3β-HSD, 17β-HSD, 17α-Hyd, and 20α-Hyd, mRNA levels of Cyp11a1, Cyp17a1, and Star, and quantity of Leydig cells in four groups. Overall, these data showed that chronic copper exposure led to copper residues in the testes, and the doses of 100 and 150 mg/kg/day copper sulfate may induce hypospermatogenesis by increasing apoptosis without affecting testosterone secretion.

中文翻译：

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慢性铜暴露通过增加细胞凋亡而不会影响睾丸激素分泌来诱导小鼠高精子发生。

慢性铜暴露会损害成年雄性小鼠的精子发生。这项研究的目的是确定慢性铜暴露是否可以通过干扰成年雄性小鼠的睾丸激素合成来诱导睾丸细胞凋亡和精子发生不足。在本研究中，将60只CD-1雄性小鼠随机分为四组，分别以0、25、100和150 mg / kg / day的剂量用硫酸铜经口管饲法连续给药8周。 。我们确定了血清和睾丸铜的含量，睾丸系数，睾丸组织病理学，精子数量和运动力，Caspase-3，Bax和Bcl-2的mRNA和蛋白水平，莱迪格细胞计数，睾丸激素含量，睾丸激素合成酶和睾丸激素合成相关基因。结果表明，血清铜水平呈剂量依赖性增加，睾丸铜水平与血清​​铜水平显着相关。给予硫酸铜100和150剂量组的雄性小鼠的精子活力和精子数量显着降低，并且睾丸损伤增加，而四组中的睾丸系数没有显着变化。在150个剂量组中，Bcl-2的mRNA水平降低，而Caspase-3则升高，在两个较高剂量组中，Bax升高。同时，在150个剂量组中，Caspase-3和Bax蛋白增加，而在三个铜处理组中，Bcl-2蛋白下降。不过，3β-HSD，17β-HSD，17α-Hyd和20α-Hyd的睾丸激素含量和睾丸激素合成酶水平，Cyp11a1，Cyp17a1，和星，以及四组Leydig细胞的数量。总体而言，这些数据表明长期暴露于铜会导致睾丸中的铜残留，而100和150 mg / kg /天的硫酸铜剂量可能会通过增加细胞凋亡而不影响睾丸激素分泌来诱导精子生成不足。