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Sulfur mustard-induced acute lung injury: Mechanistic insights into oxidative stress and inflammatory response
Zifeng Deng1, Minjie Shi2, Zhengyuan Zhao2
1Department of Toxicology, The Shaanxi Provincial Key Laboratory of Free Radical Biology and Medicine, The Shaanxi Provincial Key Laboratory of Environmental Health Hazard Assessment and Protection, The Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, School of Public Health, The Fourth Military Medical University, Shaanxi Province 710032, China; Fifth Battalion, School of Basic Medical Sciences, The Fourth Military Medical University, Shaanxi Province 710032, China.
Abstract:
Sulfur mustard (SM), a highly toxic vesicant chemical warfare agent, can induce severe acute lung injury and poses a substantial threat to human health. Oxidative stress and inflammatory responses play central roles in the pathogenesis of SM-induced lung injury, and these two processes interact in complex and mutually reinforcing ways. This review systematically summarizes recent research advances and elucidates the role of oxidative stress in SM-induced pulmonary injury from three key aspects: oxidative stress-mediated DNA damage, the stimulation of inflammatory cytokine production, and cellular apoptosis. In addition, the major components of the inflammatory response are examined, including inflammatory cell activation and infiltration, the release of inflammatory mediators, and the ability of inflammation to further amplify oxidative stress. Building on this foundation, the mechanisms underlying the interaction between oxidative stress and inflammatory responses are discussed in depth from three perspectives: ROS/RNS-mediated crosstalk, regulation of signal transduction pathways, and interactions within apoptotic signaling pathways. This review aims to provide a conceptual framework for advancing the mechanistic understanding of SM-induced lung injury and to support the development of effective therapeutic strategies.

