细微和超细颗粒物的神经毒性:使用毒性路径导向的不良结果路径框架进行全面审查
Shuang-Jian Qin1, Qing-Guo Zeng1, Hui-Xian Zeng1
1Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou 510080, China.
The Science of the total environment
|July 5, 2024
概括
细颗粒物 (PM2.5) 和超细颗粒物 (UFP) 伤害大脑. 这项研究构建了不良结果途径 (AOP) 来映射PM诱导的神经毒性机制,确定神经炎症作为关键事件.
科学领域:
- 环境健康科学 环境健康科学
- 毒理学 毒理学 毒理学
- 神经科学是一个神经科学.
背景情况:
- 细颗粒物 (PM2.5) 和超细颗粒物 (UFP) 与神经毒性和神经疾病有关.
- 由于不同的研究模型和终点,导致PM诱导的神经毒性的确切机制尚不清楚.
- 不良结果路径 (AOP) 框架提供了一种系统的方法来阐明污染物诱导的毒性机制.
研究的目的:
- 为PM2.5和UFP构建AOP,以了解它们的神经毒性机制.
- 为了确定关键的分子启动事件 (MIE) 和PM诱导的神经毒性的下游途径.
- 推进对空气中的污染物影响大脑健康的风险评估方法.
主要方法:
- 对65项关于PM2.5和UFP神经毒性研究的系统文献综述.
- 比较毒基因组学数据库 (CTD) 用于识别PM作为压力因素.
- 发明性路径分析 (IPA) 和上游调节器分析 (URA) 来确定毒性路径和启动事件.
主要成果:
- 神经炎症信号和葡萄糖皮质体受体信号被确定为常见的毒性途径.
- 神经炎症被证实是最有可能发生的分子发起事件 (MIE).
- 与PM2.5相比,对UFPs观察到明显的下游通路激活序列,突出显示UFPs的脂质代谢,线粒体功能障碍和BBB损伤.
结论:
- 这项研究提出了PM2.5和UFP的新型AOP框架,详细介绍了导致神经毒性的途径级联反应.
- 这些发现促进了对PM诱导的神经毒性和风险评估的理解.
- 基于途径的方法为开发其他环境化学品的AOP提供了基础.
相关概念视频
Types of Toxins
1.7K
Humans continually engage with an environment rich in potentially harmful chemicals. These are introduced to our bodies through inhalation, ingestion, or skin contact. These chemicals exist in various forms, such as air and environmental pollutants, agricultural chemicals, organic solvents, and heavy metals.
Air pollutants, primarily gases, pose significant threats to respiratory health, leading to conditions like hypoxia, lung cancer, and in extreme cases, death.
Environmental pollutants like...
Air pollutants, primarily gases, pose significant threats to respiratory health, leading to conditions like hypoxia, lung cancer, and in extreme cases, death.
Environmental pollutants like...
1.7K
Drugs Affecting Neurotransmitter Synthesis
1.3K
Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase,...
1.3K
Chronic Obstructive Pulmonary Disease-II: Pathophysiology
2.8K
Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
Chronic Inflammation
2.8K
Local Anesthetics: Adverse Effects
404
While local anesthetics are generally safe and well-tolerated, they can occasionally cause adverse effects that vary in severity. Local anesthetics can induce toxicity at two distinct levels. They can either produce local effects through direct contact with the neural elements or be absorbed into the bloodstream from the injection site, leading to systemic effects.
Once absorbed into the systemic circulation, local anesthetics can affect the organs that depend on the functioning of sodium...
Once absorbed into the systemic circulation, local anesthetics can affect the organs that depend on the functioning of sodium...
404


