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短链甲可以通过AIM2-和NLRP12-PANoptosome诱导小鼠的卵巢损伤

Mingxin Bai¹, Jiawei Lei¹, Fan Li¹

¹Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, Department of Preventive Medicine, Medical school, Hunan Normal University, Changsha, Hunan 410013, China.

Environmental science & technology

|January 4, 2025

概括

短链甲 (SCCPs) 剂量为0.1 mg/kg/day或更高的小鼠受损的卵巢功能. SCCPs诱导了PANoptosis和氧化应激,影响女性生殖系干细胞和荷尔蒙水平.

科学领域:

环境毒理学环境毒理学
生殖毒理学生殖毒理学
细胞生物学细胞生物学

背景情况:

短链化 (SCCP) 是具有潜在健康风险的环境污染物.
有限的研究存在于低水平的SCCP暴露对哺乳动物卵巢功能的影响.
了解SCCP诱导的生殖毒性对于公共卫生风险评估至关重要.

研究的目的:

研究口服SCCP对雌性小鼠卵巢损伤的影响.
为了确定SCCP暴露和卵巢毒性之间的剂量反应关系.
阐明SCCP诱导的卵巢功能障碍背后的细胞机制.

主要方法:

雌性ICR小鼠被口服SCCP,剂量为0,0.01,0.1和1.0毫克/公斤/天,持续21天.
收集了血清和卵巢组织进行分析.
评估了卵巢毛囊数量,氧化应激标志物,激素水平 (E2,抗穆勒激素),PANoptosis,AIM2和NLRP12 PANoptosome表达,以及女性生殖系干细胞 (FGSC) 标志物.

主要成果:

每天≥0.1 mg/kg的SCCP减少了卵巢卵泡数量,并诱导了剂量依赖的氧化应激.
在接受SCCP治疗的小鼠中,血清E2和卵巢抗穆勒尔激素水平下降.
暴露于SCCP增加了卵巢中的细胞PANoptosis,提高了AIM2-和NLRP12-PANoptosome水平,并损害了FGSCs,减少了它们的标记物表达.

结论:

在小鼠中,SCCP的口服剂量≥0.1 mg/kg/天抑制了卵巢功能.
由SCCP诱导的卵巢毒性与PANoptosis,氧化应激和对雌性生殖系干细胞的损伤有关.
这些发现表明,SCCP可能通过在卵巢细胞中诱导AIM2-和NLRP12-PANoptosome而构成生殖风险.

关键词:

这就是PANoptosis.这就是PAN光体.雌性生殖系干细胞是女性的生殖系干细胞.卵巢卵巢是一个卵巢.短链的化抛油.

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