Medicinal Safety Research Laboratories, Daiichi Sankyo Co. Ltd., 717 Horikoshi, Fukuroi, Shizuoka 437-0065, Japan.
Reprod Toxicol. 2011 May;31(4):440-6. doi: 10.1016/j.reprotox.2010.12.007. Epub 2010 Dec 23.
Mechanism mediating the testicular toxicity induced by CS-003, a triple neurokinin receptor antagonist, was investigated in male dogs. Daily CS-003 administrations showed testicular toxicity, such as a decrease in the sperm number, motility and prostate weight; and an increase in sperm abnormality, accompanying histopathological changes in the testis, epididymis and prostate. A single CS-003 administration suppressed plasma testosterone and LH levels in intact and castrated males. The suppressed LH release was restored by GnRH agonist injection, suggesting that pituitary sensitivity to GnRH is not impaired by CS-003. Treatment with SB223412, a neurokinin 3 receptor antagonist, caused a similar effect to CS-003, such as toxicity in the testis, prostate and epididymis and decreased plasma level of LH and testosterone. In conclusion, CS-003-induced testicular toxicity is caused by the inhibition of neurokinin B/neurokinin 3 receptor signaling probably at the hypothalamic level in male dogs.
我们研究了三重神经激肽受体拮抗剂 CS-003 引起雄性犬睾丸毒性的作用机制。每日 CS-003 给药可导致睾丸毒性,如精子数量、活力和前列腺重量减少;精子畸形增加,伴随睾丸、附睾和前列腺的组织病理学变化。单次 CS-003 给药可抑制完整和去势雄性动物的血浆睾酮和 LH 水平。用 GnRH 激动剂注射可恢复抑制的 LH 释放,表明 CS-003 不损害垂体对 GnRH 的敏感性。神经激肽 3 受体拮抗剂 SB223412 的治疗可引起与 CS-003 类似的作用,如睾丸、前列腺和附睾毒性以及 LH 和睾酮的血浆水平降低。总之,CS-003 引起的睾丸毒性是由神经激肽 B/神经激肽 3 受体信号的抑制引起的,可能发生在雄性犬的下丘脑水平。