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Arsenic-induced lung inflammation and fibrosis in a rat model: Contribution of the HMGB1/RAGE, PI3K/AKT, and TGF-β1/SMAD pathways
2021, Toxicology and Applied PharmacologyCitation Excerpt :Experimental animal studies have shown that arsenic exposure can lead to disturbed immune homeostasis and inflammatory responses in the lungs of rats (Li et al., 2017). In terms of arsenic-induced lung injury, the main mechanistic hypotheses currently include arsenic-related respiratory immune impairment (Duan et al., 2017), reduced pathogen clearance due to impaired function of alveolar macrophages(Gulyas et al., 1990), and changes to airway proteomic expression profiles in mice and humans (Lantz et al., 2007). However, the specific molecular mechanisms underlying arsenic-induced lung injury have not been fully elucidated.
Fly ash: Safety and health issues
2021, Handbook of Fly AshRespiratory burst in alveolar macrophages exposed to urban particles is not a predictor of cytotoxicity
2013, Toxicology in VitroCitation Excerpt :Similar observations have been made by others with metal oxides and their adverse biological activity in vitro, and the effects have been attributed to the ability of insoluble components to generate intracellular oxidative stress (Ghio et al., 1999; Labedzka et al., 1989; Schluter et al., 1995). Examples of differential activity of metal oxides include iron III oxide-mediated induction of anti-inflammatory state in rat alveolar macrophages (Beck-Speier et al., 2009) and inhibition of NADPH oxidase activity in bovine alveolar macrophages exposed to copper II oxide (Gulyas et al., 1990) both due to the high intracellular dissolution of the metal oxides, and low cytotoxicity of nickel oxide in canine and rodent alveolar macrophages due to its poor intracellular dissolution (Benson et al., 1986). The patterns of effects of particles on the respiratory burst of rat alveolar macrophages in the current study were similar across the three stimulants employed.