PDF(Pubmed)
Abstract：
This work aimed to elucidate how O3 pollution causes a loss of regulation in the immune response in both the brain and the intestine. In this work, we studied the effect of exposing rats to low doses of O3 based on the association between the antioxidant response of superoxide dismutase (SOD) levels and the nuclear factor kappa light chains of activated B cells (NFκB) as markers of inflammation. Method: Seventy-two Wistar rats were used, divided into six groups that received the following treatments: Control and 7, 15, 30, 60, and 90 days of O3. After treatment, tissues were extracted and processed using Western blotting, biochemical, and immunohistochemical techniques. The results indicated an increase in 4-hydroxynonenal (4HNE) and Cu/Zn-SOD and a decrease in Mn-SOD, and SOD activity in the substantia nigra, jejunum, and colon decreased. Furthermore, the translocation of NFκB to the nucleus increased in the different organs studied. In conclusion, repeated exposure to O3 alters the regulation of the antioxidant and inflammatory response in the substantia nigra and the intestine. This indicates that these factors are critical in the loss of regulation in the inflammatory response; they respond to ozone pollution, which can occur in chronic degenerative diseases.
摘要：
这项工作旨在阐明O3污染如何导致大脑和肠道免疫反应的调节丧失。在这项工作中,我们基于超氧化物歧化酶（SOD）水平的抗氧化反应与活化B细胞（NFκB）的核因子κ轻链之间的关联，研究了将大鼠暴露于低剂量O3的作用。方法:采用72只Wistar大鼠,分成6组,接受以下处理:对照和7、15、30、60和90天的O3。治疗后,使用蛋白质印迹法提取和处理组织，生物化学，和免疫组织化学技术。结果表明4-羟基壬烯醛（4HNE）和Cu/Zn-SOD的增加和Mn-SOD的减少，黑质中的SOD活性，空肠,结肠减少。此外，在研究的不同器官中，NFκB向细胞核的易位增加。总之,反复暴露于O3会改变黑质和肠道中抗氧化剂和炎症反应的调节。这表明这些因素在炎症反应中失去调节是至关重要的；它们对臭氧污染有反应，可发生在慢性退行性疾病中。
