Toxicological Effects of Artificial Fine Particulate Matter in Rats through Induction of Oxidative Stress and Inflammation

Abstract

Airborne fine particulate matter with an aerodynamic diameter equal to or smaller than 2.5 μm (abbreviated as PM 2.5 ) increases the risk of nasal lesions, but the underlying molecular mechanism has not been fully elucidated. In the atmosphere, the composition of PM 2.5 collected varies in physical and chemical properties, which affects its damage to human health. Thus, we constructed artificial PM 2.5 particles based on actual PM 2.5 and investigated the in vivo effects of artificial PM 2.5 exposure on the oxidative stress, inflammatory response, and nasal mucosa morphology of rats. The results showed that artificial PM 2.5 is comparable in composition ratio, size, and morphology to actual PM 2.5 . This in vivo study indicated that artificial PM 2.5 exposure reduces total superoxide dismutase and glutathione peroxidase activities, elevates malondialdehyde content in the nasal mucosa, and induces increased levels of pro-inflammatory mediators, including interleukin-1, interleukin-6 and tumor necrosis factor-α. Our data shows that artificial PM 2.5 particles could be used for experimental study of PM 2.5 toxicology, ensuring that the physical and chemical properties of experimental PM 2.5 are relatively constant and allowing for repeatability of this research. Oxidative damage and inflammatory response may be the toxic mechanisms that cause nasal lesions after exposure to artificial PM 2.5 .

The Relationship between Fine Particle Matter (PM2.5) Exposure and Upper Respiratory Tract Diseases

“…Guo et al demonstrated similar results in NLF collected from healthy rats exposed to PM2.5, which contained higher levels of IL-4, IL-13, and TGF-β1 compared to the control NLF [25]. Also, Hong et al showed that PM2.5 increased IL-1, IL-6, and TNF-α levels in the nasal mucosa of rats [36].…”

“…Interestingly, the levels of nuclear factor erythroid 2-related factor 2 (Nrf2), a key regulator of cellular oxidant resistance, were increased in the nucleus and decreased in the cytoplasm after PM2.5 treatment, suggesting that the nuclear translocation of Nrf2 was inhibited [35,37]. Analogous to these findings, Hong et al demonstrated that GSH-Px was downregulated in the nasal mucosa of rats exposed to PM2.5 and Gu et al demonstrated that PM2.5 exposure decreased GSH and increased MDA levels in human nasal epithelial cells [36,38].…”

“…One of them is the alteration of antioxidant enzyme activity. Several studies confirmed that PM2.5 exposure reduced superoxide dismutase (SOD) activity and increased the level of the oxidative stress marker malondialdehyde (MDA) in the nasal mucosa [25,35,36]. Moreover, Hong et al demonstrated that RPMI 2650 cells exposed to PM2.5 exhibited decreased activity of other antioxidant enzymes such as catalase (CAT) and glutathione peroxidase (GSH-Px).…”

Causal relationship between particulate matter and COVID-19 risk: A mendelian randomization study

“…Consequently, the adaptive viral defence system is hampered, potentially leading to dysregulated immunopathological process in COVID-19 [ 41 , 42 ]. Exposure of PM2.5 has been associated with increased levels of reactive oxygen species (ROS) and the release of multiple proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α), interleukin-1 (IL-1), and interleukin-6 (IL-6) [ 43 , 44 ]. Notably, oxidative stress plays a crucial role in COVID-19, with excessive ROS generation contributing to the onset of cytokine storms.…”

Causal relationship between particulate matter 2.5 and hypothyroidism: A two-sample Mendelian randomization study

“…Previous studies have reported that increased traffic-related PM 2.5 concentrations are associated with altered responses to inflammatory markers (51). Animal experiments have found that artificial PM 2.5 exposure can induce increased levels of interleukin (IL)-1, IL-6 and tumor necrosis factor α (TNFα) in rats, thereby increasing the risk of nasal lesions (52). Hypothyroidism is associated with disturbed cytokine concentrations, an abundance of reactive oxygen species (ROS), and altered signal transduction in most parts of the brain (53).…”