Veronesi Bellina, Makwana Om, Pooler Melanie, Chen Lung Chi
National Health and Environmental Effects Research Laboratory, Neurotoxicology Division, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina 27711, USA.
Inhal Toxicol. 2005 Apr;17(4-5):235-41. doi: 10.1080/08958370590912888.
This study reports that subchronic exposure of Tuxedo, NY concentrated ambient particulates (CAPs) produces neuropathological damage in the brains of Apo E-deficient mice (Apo E-/-). These genetically modified mice are characterized by elevated levels of oxidative stress (OS) in the brain. Microscopic examination of coronal sections of the brain, immunocytochemically stained for dopamineric neurons, indicated that neurons from the substantia nigral nucleus compacta were significantly reduced by 29% in CAPs-exposed Apo E-/- mice relative to air-exposed Apo E-/- controls. In addition, statistically significant increases (p < .05) in immunocytochemically stained astrocytes were noted. The dopaminergic neurons of the nucleus compact are specifically targeted in Parkinson's disease. The present study expands the systems affected by particulate matter to include the brain, and supports an environmental role for the development of neurodegeneration in OS-susceptible individuals.
本研究报告称,纽约州塔克斯多市的浓缩环境颗粒物(CAPs)亚慢性暴露会在载脂蛋白E缺乏小鼠(Apo E-/-)的大脑中产生神经病理损伤。这些基因改造小鼠的特征是大脑中的氧化应激(OS)水平升高。对大脑冠状切片进行显微镜检查,并对多巴胺能神经元进行免疫细胞化学染色,结果表明,与暴露于空气的Apo E-/-对照小鼠相比,暴露于CAPs的Apo E-/-小鼠黑质致密部的神经元显著减少了29%。此外,免疫细胞化学染色的星形胶质细胞有统计学意义的增加(p <.05)。致密核的多巴胺能神经元是帕金森病的特定靶点。本研究将受颗粒物影响的系统扩展至大脑,并支持在对OS敏感的个体中,环境因素在神经退行性变发展中的作用。