Rivas-Arancibia Selva, Rodríguez-Martínez Erika, Valdés-Fuentes Marlen, Miranda-Martínez Alfredo, Hernández-Orozco Eduardo, Reséndiz-Ramos Citlali
Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico.
Antioxidants (Basel). 2024 Apr 27;13(5):536. doi: 10.3390/antiox13050536.
This work aimed to elucidate how O 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 O 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 O. 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 O 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.
这项研究旨在阐明臭氧污染如何导致大脑和肠道免疫反应的调节失衡。在本研究中,基于超氧化物歧化酶(SOD)水平的抗氧化反应与活化B细胞核因子κB轻链(NFκB)作为炎症标志物之间的关联,我们研究了低剂量臭氧暴露对大鼠的影响。方法:使用72只Wistar大鼠,分为六组,分别接受以下处理:对照组以及臭氧暴露7、15、30、60和90天。处理后,使用蛋白质免疫印迹、生化和免疫组织化学技术提取并处理组织。结果表明,4-羟基壬烯醛(4HNE)和铜/锌超氧化物歧化酶增加,锰超氧化物歧化酶减少,黑质、空肠和结肠中的超氧化物歧化酶活性降低。此外,在所研究的不同器官中,NFκB向细胞核的转位增加。总之,反复暴露于臭氧会改变黑质和肠道中抗氧化和炎症反应的调节。这表明这些因素在炎症反应调节失衡中至关重要;它们对臭氧污染有反应,而臭氧污染可能发生在慢性退行性疾病中。