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锰暴露导致雄性小鼠生殖毒性,涉及前列腺素 E2 受体 EP1 和 EP2 通过下丘脑 GnRH 分泌的激活。

Manganese exposure caused reproductive toxicity of male mice involving activation of GnRH secretion in the hypothalamus by prostaglandin E2 receptors EP1 and EP2.

机构信息

Department of Environmental Health, School of Public Health, China Medical University, Shenyang, People's Republic of China; Department of Medical, Second Affiliated Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, People's Republic of China.

Department of Environmental Health, School of Public Health, China Medical University, Shenyang, People's Republic of China; Department of Occupational Diseases, Linyi People's Hospital, Shandong, People's Republic of China.

出版信息

Ecotoxicol Environ Saf. 2020 Sep 15;201:110712. doi: 10.1016/j.ecoenv.2020.110712. Epub 2020 Jun 5.

DOI:10.1016/j.ecoenv.2020.110712
PMID:32502905
Abstract

Exposure to manganese (Mn) can cause male reproductive damage and lead to abnormal secretion of sex hormones. Gonadotropin-releasing hormone (GnRH) plays an important role in the neuromodulation of vertebrate reproduction. Astrocytes can indirectly regulate the secretion of GnRH by binding paracrine prostaglandin E (PGE) specifically to the EP1 and EP2 receptors on GnRH neurons. Prior studies assessed the abnormal secretion of GnRH caused by Mn exposure, but the specific mechanism has not been reported in detail. This study investigated the effects of Mn exposure on the reproductive system of male mice to clarify the role of PGE in the abnormal secretion of GnRH in the hypothalamus caused by exposure to Mn. Our data demonstrate that antagonizing the EP1 and EP2 receptors of PGE can restore abnormal levels of GnRH caused by Mn exposure. Mn exposure causes reduced sperm count and sperm shape deformities. These findings suggest that EP1 and EP2, the receptors of PGE, may be the key to abnormal GnRH secretion caused by Mn exposure. Antagonizing the PGE receptors may reduce reproductive damage caused by Mn exposure.

摘要

暴露于锰(Mn)可能会导致男性生殖系统受损,并导致性激素分泌异常。促性腺激素释放激素(GnRH)在脊椎动物生殖的神经调节中起着重要作用。星形胶质细胞可以通过与 GnRH 神经元上的 EP1 和 EP2 受体特异性结合旁分泌前列腺素 E(PGE),间接地调节 GnRH 的分泌。先前的研究评估了 Mn 暴露引起的 GnRH 异常分泌,但具体机制尚未详细报道。本研究探讨了 Mn 暴露对雄性小鼠生殖系统的影响,以阐明 PGE 在 Mn 暴露引起的下丘脑 GnRH 异常分泌中的作用。我们的数据表明,拮抗 PGE 的 EP1 和 EP2 受体可以恢复 Mn 暴露引起的 GnRH 异常水平。Mn 暴露导致精子数量减少和精子形状畸形。这些发现表明,PGE 的 EP1 和 EP2 受体可能是 Mn 暴露引起 GnRH 异常分泌的关键。拮抗 PGE 受体可能会减少 Mn 暴露引起的生殖损伤。

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Manganese exposure caused reproductive toxicity of male mice involving activation of GnRH secretion in the hypothalamus by prostaglandin E2 receptors EP1 and EP2.锰暴露导致雄性小鼠生殖毒性,涉及前列腺素 E2 受体 EP1 和 EP2 通过下丘脑 GnRH 分泌的激活。
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