In recent years, with the acceleration of industrialization, the decline of male fertility caused by heavy metal pollution has attracted much attention. However, whether the inhibition of testicular function after cadmium exposure is reversible remains to be studied. In this study, we constructed rat models of cadmium exposure and dis-exposure, and collected relative samples to observe the changes of related indicators. The results showed that cadmium exposure could reduce the fertility, inhibit the hypothalamic-pituitary-testis axis and activate hypothalamic-pituitary-adrenal axis function, the testicular signal was abnormal, cell proliferation was inhibited and apoptosis was enhanced. Four weeks after the exposure was stopped, the fertility was still decreased, testicular testosterone synthesis and spermatogenesis were inhibited, cell proliferation was inhibited and apoptosis was enhanced, but all of them were reversed. After eight weeks of cadmium exposure, the above indicators were observed to return to normal. At the same time, by giving different concentrations of corticosterone to spermatogonium, we confirmed that corticosterone may regulate the proliferation and apoptosis of spermatogonium through signal. In this study, the reproductive toxicity of cadmium, a metal environmental pollutant, was analyzed in depth to provide a new theoretical and experimental basis for ensuring male reproductive health.

中文翻译：

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镉暴露后睾丸功能障碍及其“恢复作用”

近年来，随着工业化进程的加快，重金属污染导致的男性生育能力下降备受关注。然而，镉暴露后对睾丸功能的抑制是否可逆仍有待研究。本研究构建大鼠镉暴露和脱暴露模型，并采集相关样本观察相关指标的变化。结果表明，镉暴露可降低生育能力，抑制下丘脑-垂体-睾丸轴，激活下丘脑-垂体-肾上腺轴功能，使睾丸信号异常，细胞增殖受到抑制，细胞凋亡增强。停止照射4周后，生育能力仍下降，睾丸睾酮合成和精子发生受到抑制，细胞增殖受到抑制，细胞凋亡增强，但均得到逆转。镉暴露八周后，观察上述指标恢复正常。同时，通过给予精原细胞不同浓度的皮质酮，我们证实皮质酮可能通过信号调节精原细胞的增殖和凋亡。本研究深入分析金属环境污染物镉的生殖毒性，为保障男性生殖健康提供新的理论和实验依据。