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Effects of the air pollution on the decreased P53, Nrf2 and HO-1 protein levels along with tissue damage caused by oxidative stress in the lung of rat as an animal model | ||
| Caspian Journal of Environmental Sciences | ||
| مقالات آماده انتشار، اصلاح شده برای چاپ، انتشار آنلاین از تاریخ 10 تیر 1402 اصل مقاله (950.43 K) | ||
| نوع مقاله: Research Paper | ||
| شناسه دیجیتال (DOI): 10.22124/cjes.2023.6825 | ||
| نویسندگان | ||
| Mahdi Farhadi1؛ Pejman Mortazavi* 2؛ Saeed Motesaddi Zarandi3؛ Akram Eidi1 | ||
| 1Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran | ||
| 2Department of Pathobiology, Science and Research Branch, Islamic Azad University, Tehran, Iran | ||
| 3Department of Environmental Health Engineering, School of Public Health and Safety, Shahid Beheshti University of Medical Sciences, Tehran, Iran | ||
| چکیده | ||
| Air pollution is associated with respiratory pathologies, and exposure to airborne particles with an aerodynamic diameter of 2.5 microns (PM2.5) is a significant risk factor for respiratory patients. This study aimed to investigate the effects of PM2.5 exposures on lung tissue pathology and the function of antioxidant enzymes in a rat animal model. The animals were exposed to PM2.5 for two different periods: 3 and 6 months, with a frequency of 4 days per week and a duration of 5 hours (from 9.00 am to 14.00 pm) per day. The activity of antioxidant enzymes, as well as lung histology and the protein expression of p53, Nrf2, and HO-1, were assessed in the lung tissue of the exposed rats. The results revealed a significant increase in malondialdehyde (MDA) levels and a significant decrease in antioxidant enzymes (CAT, SOD, and GPx) in the animals exposed to PM2.5. Moreover, a noticeable reduction in the protein levels of p53, Nrf2, and HO-1 was observed in the lung tissues of the rats after PM2.5 exposure, which was accompanied by pathological changes. In conclusion, PM2.5 exposure leads to severe damage to lung tissue by reducing the activity of antioxidant enzymes and inducing oxidative stress through the activation of Nrf2 and P53 signalling pathways. | ||
| کلیدواژه‌ها | ||
| Air pollution؛ P53؛ Nrf2؛ HO-1؛ Oxidative stress؛ Lung damage | ||
| مراجع | ||
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