Exposure to Ozone Increases Executing Caspases 3 and 8 and Downregulates Bcl-2 in the Hippocampus, Frontal Cortex, and Cerebellum of Rats

Abstract Ozone (O3) stands as one of the most prevalent atmospheric pollutants, arising from a photochemical reaction between volatile organic compounds (VOC), nitrogen oxides (NOx), and sunlight. According to the World Health Organization (WHO), exposure to O3 levels above 100 g/m3 for 8 hours or longer proves harmful. O3 triggers oxidative stress, resulting in lipid oxidation, inflammation, alterations in metabolic and cellular signaling, and potentially initiating cell death in vulnerable brain regions. Both, inflammation, and oxidative stress are recognized for their capacity to induce cell death, primarily through the apoptosis pathway. Apoptosis is programmed cell death characterized by caspase activation, DNA fragmentation, and the formation of apoptotic bodies. Various proteins intervene in this process along two pathways: intrinsic and extrinsic. This study aims to identify the expression of pro-apoptotic proteins and Bcl-2 in the frontal cortex, cerebellum, and hippocampus of rats exposed to O3 acutely. Methodology: Two groups of twenty Wistar rodents (250-300 g) were established. The control group (n=10) was exposed to unrestricted polluted air for 12 hours, while the experimental group (n=10) was exposed to 1 ppm of O3. After exposure, the animals were sacrificed for immunofluorescence and Western blot analysis. Using a t-test, the arbitrary units of pro-apoptotic proteins and Bcl-2 were compared between the two groups. Results and Conclusions: The investigation unveiled notable discrepancies in caspase-3 and 8, Bcl-2, and TUNEL. These findings lead us to conclude that acute O3 exposure induces apoptosis in the hippocampus, cerebellum, and frontal cortex primarily via the extrinsic pathway.