摘要
百草枯(paraquat,PQ)是一种有机杂环类非选择性除草剂,由于廉价且有效而得到广泛应用。我国百草枯中毒的患病率在过去的几年内急剧增加。自服或误服PQ导致中毒成为我国普遍存在的一个公共卫生问题。PQ吸收入组织产生大量自由基介导氧化应激,造成线粒体功能障碍,导致的急性呼吸窘迫综合征(acute respiratory distress sydrome,ARDS),后期导致肺纤维化、神经功能障碍等。有报告称PQ死亡率在90%以上。具体毒理机制仍不清楚。本文回顾、总结了PQ致急性肺损伤的分子机制的研究进展。
Paraquat(PQ),a non-selective organic heterocyclic herbicide,is widely used because of its low cost and efficiency.The prevalence of PQ poisoning in China has increased dramatically in the past few years.PQ Poisoning caused by self-administration or accidental administration has become a common public health problem in China.PQ is absorbed and a large number of free radicals are produced,which mediate oxidative stress and result in mitochondrial dysfunction.Acute respiratory distress syndrome(ARDS) occurs and later leads to pulmonary fibrosis,neurological disorder etc.It has been reported that the mortality of PQ is more than 90%.The specific toxicological mechanism remains unclear.This article reviewed and summarized the research progress of molecular mechanisms on ARDS caused by PQ poisoning.
出处
《武警后勤学院学报(医学版)》
CAS
2017年第11期1000-1004,共5页
Journal of Logistics University of PAP(Medical Sciences)
基金
武警后勤学院附属医院种子基金项目(WYB201113)
关键词
百草枯
自由基
线粒体功能障碍
分子机制
急性呼吸窘迫综合征
Paraquat
Free radicals
Mitochondrial dysfunction
Molecular mechanism
Acute respiratory distress syndrome