Reddy Annem Ravi Teja, Mahadik Sakshi Ramesh, Choudhary Khushboo, Pothuraju Naresh, Singh Sanjiv, Murti Krishna, Ramalingam P, Kumar Nitesh
Department of Regulatory Toxicology, Industrial Area, National Institute of Pharmaceutical Education and Research, Hajipur, EPIP Campus, Hajipur, 844102, India.
Department of Pharmacology and Toxicology, Industrial Area, National Institute of Pharmaceutical Education and Research, Hajipur, EPIP Campus, Hajipur, 844102, India.
Biol Trace Elem Res. 2025 Jun 30. doi: 10.1007/s12011-025-04717-8.
Neuroinflammation is increasingly recognized as a critical factor in the progression of various neurological disorders, with chronic exposure to environmental toxicants like arsenic emerging as a major contributor. This review focuses on arsenic-induced neuroinflammation, highlighting its underlying molecular mechanisms and pathways, global epidemiological burden, and current strategies for effective management. Arsenic groundwater contamination, particularly prevalent in Asian countries, poses a significant health risk to millions across more than 100 nations. Chronic exposure to arsenic generates reactive oxygen species (ROS), triggering oxidative stress and activating microglia, the key drivers of neuroinflammation. This cascade promotes proinflammatory cytokine release, leading to cognitive and neurological impairments. This review examines the underlying mechanisms, including mitochondrial dysfunction, oxidative damage, and inflammatory signaling pathways. Additionally, this review highlights current therapeutic strategies aimed at mitigating arsenic-induced neurotoxicity, including chelation therapy, natural antioxidants, and supplementation with essential trace elements. By addressing the multifactorial mechanisms underlying arsenic-induced neuroinflammation, the review emphasizes the urgent need for integrated public health initiatives and targeted interventions to alleviate the neurological consequences of chronic arsenic exposure.
神经炎症日益被认为是各种神经系统疾病进展中的一个关键因素，长期接触砷等环境毒物是一个主要促成因素。本综述聚焦于砷诱导的神经炎症，突出其潜在的分子机制和途径、全球流行病学负担以及当前有效的管理策略。砷污染地下水在亚洲国家尤为普遍，对100多个国家的数百万人构成重大健康风险。长期接触砷会产生活性氧（ROS），引发氧化应激并激活小胶质细胞，而小胶质细胞是神经炎症的关键驱动因素。这一连串反应促进促炎细胞因子的释放，导致认知和神经功能障碍。本综述探讨了其潜在机制，包括线粒体功能障碍、氧化损伤和炎症信号通路。此外，本综述强调了当前旨在减轻砷诱导的神经毒性的治疗策略，包括螯合疗法、天然抗氧化剂以及补充必需微量元素。通过阐述砷诱导神经炎症背后的多因素机制，本综述强调迫切需要综合公共卫生举措和针对性干预措施，以减轻慢性砷暴露的神经后果。
