产前氧化暴露诱导的胎儿小鼠多个器官的形态和功能变化及其特征
Yifan Liu1, Lingbo Rong2, Ailikaiti Aihemaitijiang2
1Department of Pharmacology, Wuhan University School of Basic Medical Sciences, Wuhan 430071, China; Department of Pediatric Surgery, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
Chemico-biological interactions
|January 23, 2026
概括
在小鼠中产前氧化 (PHE) 暴露导致了不良的妊娠结果和异常的胎儿发育,影响多个器官. 这些影响可能与改变的自和亡有关,突出显示了发育性毒性风险.
科学领域:
- 生殖毒理学 生殖毒理学
- 发展生物学 发展生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 基氨酸用于自身免疫性疾病和怀孕期间.
- 关于产前氧化暴露 (PHE) 对后代发育的影响的综合数据有限.
研究的目的:
- 在小鼠中系统评估PHE的发育毒性.
- 调查PHE对怀孕结果,孕产妇和胎儿血液表型以及多器官发育的影响.
- 探索PHE诱导的发育毒性的潜在潜在机制.
主要方法:
- 在整个孕期内,怀孕的小鼠在不同的剂量 (20,40,80 mg/kg·d) 中口服氧化.
- 评估怀孕结果,母体和胎儿血液指标,胎儿器官形态和功能.
- 分析了器官功能变化,自和亡之间的相关性.
主要成果:
- PHE增加了胎儿再吸收,死胎和子宫内生长限制 (IUGR).
- 在胎儿中观察到血液指标的显著变化.
- 长骨和脏的发育受阻,上腺类固醇生成和胎盘合成;促进肺表面活性剂和胆酸合成.
- 确认长骨,生殖腺和肺部的形态异常,具有显著的性别差异和剂量依赖性.
- 女性多器官功能障碍与自和亡的增加正相关.
结论:
- PHE会导致不良妊娠结果和子女多器官发育异常.
- 潜在的机制包括抑制的自和增加的亡.
- 提供了氧化对发展毒性的证据,为危险评估和预防策略提供了信息.
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