Short-term exposure to ZnO/MCB persistent free radical particles causes mouse lung lesions via inflammatory reactions and apoptosis pathways.

Environmentally persistent free radicals (EPFRs) are easily generated in the combustion processes of municipal solid waste (MSW) and can cause adverse effects on human health. This study focuses on understanding the toxicity of EPFR particles (ZnO/MCB containing EPFRs) to human bronchial epithelial cell lines BEAS-2B and 16HBE, murine macrophages Raw264.7, and the lung of BALB/c mice after a short exposure (7 days). Exposure of BEAS-2B, 16HBE, and Raw264.7 cells to ZnO/MCB particles significantly increased the reactive oxygen species (ROS) production and perturbed levels of intracellular redox conditions (decreased the intracellular GSH level and the activity of cytosolic SOD, and stimulated oxidative stress related proteins such as HO-1 and Nrf2). EPFR particles decreased the mitochondrial membrane potential (MMP) and induced cell apoptosis, including the activation of Caspase-3, Bax, and Bcl-2 apoptotic signalling pathways. A signature inflammatory condition was observed in both cell models and the mouse model for lung lesions. Our data suggest that EPFRs in particles have greater toxicity to lung cells and tissues that are potential health hazards to human lung. Image 1 • Understand the processes of ZnO/MCB EPFRs formation at the incineration temperatures. • Understand how ZnO/MCB EPFRs induce the oxidative stress, mitochondrial membrane potential change, apoptosis, and cytokine release in three cell lines. • Reveal the adverse responses of mouse organs and tissues upon exposure to EPFRs. Capsule Abstract: ZnO/MCB EPFRs caused apoptosis of lung cells, macrophages and normal adult mouse lung tissue and other pathological conditions. ZnO/MCBs are toxic to lung cells and tissues. [ABSTRACT FROM AUTHOR]

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