暴露于环境纳米粒子与神经毒性有关

Ehsani Mojtaba, Montazeri Zeinab, Rafati Mehravar
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引用次数: 4

摘要

空气污染暴露是环境诱导的氧化应激和炎症的最普遍原因之一,这两者都与中枢神经系统(CNS)疾病有关。中枢神经系统已成为暴露于空气污染物对健康不利影响的一个重要目标,它可能导致神经和神经发育障碍。空气污染包括气体、颗粒物(PM)、超细颗粒物(ufp)、金属和有机化合物的各种成分。环境空气中PM和UFPM的一个重要来源与空气污染相关的贩运有关,主要是柴油排气颗粒(dep)。对照动物研究和流行病学研究表明,接触空气污染,特别是城市空气污染或dep,可能导致神经毒性。具体而言,暴露于空气污染物作为一个重要因素可能是神经发育障碍(如自闭症)和神经障碍(如…阿尔茨海默病(AD))。动物和人类暴露在空气污染物中最明显的影响是氧化应激和神经变性。对暴露于DEPs的大鼠的研究显示,在大脑的各个区域,特别是嗅球(OB)和海马(HI),出现了小胶质细胞活性、脂质过氧化增加和神经元积聚。成人神经发生障碍也被发现。在大多数情况下,DEP对雄性小鼠的影响更为明显,这可能是由于雄性小鼠抗氧化能力较低,对氧磷酶2的表达较少。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Neurotoxicity related exposure to ambient nanoparticles
Air pollution exposure is among the most prevalent reasons for environmentally-induced oxidative stress and inflammation, both of which are implicated in the central nervous system (CNS) diseases. The CNS has emerged as an important target for adverse health effects of exposure to air pollutants, where it can cause neurological and neurodevelopmental disorders. Air pollution includes various components of gases, particulate matter (PM), ultrafine particulate (UFPs), metals, and organic compounds. An important source of PM and UFPM in the ambient air is associated with air pollution-related trafficking, and primarily diesel exhaust particles (DEPs). Controlled animal studies and epidemiological studies show that exposure to air pollution, and in particular urban air pollution or DEPs, may lead to neurotoxicity. In specific, exposure to air pollutants as an important factor may be in neurodevelopmental disorders (eg Autism) and neurological disorders (eg.., Alzheimer’s Disease (AD)). The most noticeable effects of exposure to air pollutants in animals and humans are oxidative stress and neurodegeneration. Studies in rats exposed to DEPs showed microglial activity, increased lipid peroxidation, and neuronal accumulation in various areas of the brain, especially the olfactory bulb (OB) and the hippocampus (HI). Disorders of adult neurogenesis were also found. In most cases, the effects of DEP are more pronounced in male mice, probably due to lower antioxidant capacity due to less expression of paraoxonase 2.
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