Fagundes Lucas Sagrillo, Fleck Alan da Silveira, Zanchi Ana Claudia, Saldiva Paulo Hilário Nascimento, Rhoden Cláudia Ramos
a Laboratório de Estresse Oxidativo e Poluição Atmosférica - Universidade Federal de Ciências da Saúde de Porto Alegre - UFCSPA , Porto Alegre , RS , Brazil and.
b Laboratório de Poluição Atmosférica Experimental, Faculdade de Medicina, Universidade de São Paulo-USP , São Paulo , SP , Brazil.
Inhal Toxicol. 2015;27(10):462-7. doi: 10.3109/08958378.2015.1060278. Epub 2015 Sep 1.
Several experimental and epidemiological studies have demonstrated the neurological adverse effects caused by exposure to air pollution, specifically in relation to pollutant particulate matter (PM). The objective of this study was to investigate the direct effect of PM in increased concentrations in different brain regions, as well as the mechanisms involving its neurotoxicity, by evaluating oxidative stress parameters in vitro.
Olfactory bulb, cerebral cortex, striatum, hippocampus and cerebellum of rats were homogenized and incubated with PM < 2.5 μm of diameter (PM2.5) at concentrations of 3, 5 and 10 µg/mg of tissue. The oxidative damage caused by lipid peroxidation of these structures was determined by testing the thiobarbituric acid reactive species (TBA-RS). In addition, we measured the activity of antioxidant enzyme catalase (CAT) and superoxide dismutase (SOD).
All PM concentrations were able to damage the cerebellum and hippocampus, strongly enhancing the lipid peroxidation in both structures. PM incubation also decreased the CAT activity of the hippocampus, cerebellum, striatum and olfactory bulb, though it did not generate higher levels of lipid peroxidation in either of the last two structures. PM incubation did not alter any measurement of the cerebral cortex.
The cerebellum and hippocampus seem to be more susceptible than other brain structures to in vitro direct PM exposure assay and the oxidative stress pathway catalyzes the neurotoxic effect of PM exposure, as evidenced by high consumption of CAT and high levels of TBA-RS. Thus, PM direct exposure seems to activate toxic neurological effects.
多项实验和流行病学研究表明，接触空气污染会对神经系统产生不良影响，特别是与污染物颗粒物（PM）有关。本研究的目的是通过体外评估氧化应激参数，研究不同脑区中浓度升高的PM的直接作用及其神经毒性机制。
将大鼠的嗅球、大脑皮层、纹状体、海马体和小脑匀浆，并与直径小于2.5μm的PM（PM2.5）以3、5和10μg/mg组织的浓度孵育。通过检测硫代巴比妥酸反应性物质（TBA-RS）来确定这些结构脂质过氧化引起的氧化损伤。此外，我们还测量了抗氧化酶过氧化氢酶（CAT）和超氧化物歧化酶（SOD）的活性。
所有PM浓度均能损伤小脑和海马体，强烈增强这两个结构中的脂质过氧化。PM孵育还降低了海马体、小脑、纹状体和嗅球的CAT活性，尽管在最后两个结构中均未产生更高水平的脂质过氧化。PM孵育未改变大脑皮层的任何测量结果。
小脑和海马体似乎比其他脑结构更容易受到体外直接PM暴露试验的影响，氧化应激途径催化了PM暴露的神经毒性作用，CAT的高消耗和高TBA-RS水平证明了这一点。因此，PM直接暴露似乎会激活有毒的神经学效应。
