最近对二-2-乙烯基) - 甲酸盐的毒理学研究取得了进展:专注于内质网膜应激通路的研究
Jiten Singh1, Ashok Jangra1, Dinesh Kumar1
1Department of Pharmaceutical Sciences, School of Interdisciplinary and Applied Sciences, Central University of Haryana, Mahendergarh, 123031, Haryana, India.
Chemosphere
|April 9, 2024
概括
暴露于二--2-乙烯基) - 甲酸盐 (DEHP) 增塑剂会通过内分泌网膜 (ER) 应激引起器官毒性. 这次审查详细介绍了DEHP的细节.
科学领域:
- 环境健康 环境健康
- 毒理学 毒理学 毒理学
- 细胞生物学 细胞生物学
背景情况:
- 2-乙烯基) - 酸盐 (DEHP) 是一种广泛使用的增塑剂,在众多消费品和医疗产品中发现.
- DEHP从重复使用的产品中漏,导致广泛的环境发生和人类暴露.
- 暴露于DEHP与通过多种生物途径在各种器官中产生毒性有关.
研究的目的:
- 审查DEHP诱导毒性的机制,重点关注内分泌网膜 (ER) 应激通路.
- 探索其他涉及的途径,包括PPAR相关的信号,氧化应激,炎症和线粒体平衡.
- 总结最近关于DEHP毒性的发现和针对ER压力的潜在药理干预措施.
主要方法:
- 关于DEHP诱导毒性的最近研究的文献综述.
- 对研究的分析,重点是内质网膜 (ER) 应激途径.
- 收集关于替代机制和药理干预措施的数据.
主要成果:
- 暴露于DEHP显著诱导内质网膜 (ER) 应激,影响蛋白质合成和折叠.
- ER压力与丸,大脑,肺部,脏,心脏和肝脏的DEHP毒性有关.
- 其他关键机制包括氧化应激,炎症和破坏平衡.
结论:
- 在全球范围内,DEHP暴露对健康构成重大风险,其介于ER压力和其他细胞干扰.
- 了解这些途径为减轻DEHP诱导的毒性提供了目标.
- 针对ER压力的药理干预措施在解决DEHP毒性方面显示出希望.
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