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铁死亡在环境诱导的神经毒性中的作用。

Ferroptosis implication in environmental-induced neurotoxicity.

机构信息

School of Life Sciences, Fudan University, Shanghai 200438, China; Wanchuanhui (Shanghai) Medical Technology Co., Ltd, Shanghai 201501, China.

出版信息

Sci Total Environ. 2024 Jul 15;934:172618. doi: 10.1016/j.scitotenv.2024.172618. Epub 2024 Apr 24.

DOI:10.1016/j.scitotenv.2024.172618
PMID:38663589
Abstract

Neurotoxicity, stemming from exposure to various chemical, biological, and physical agents, poses a substantial threat to the intricate network of the human nervous system. This article explores the implications of ferroptosis, a regulated form of programmed cell death characterized by iron-dependent lipid peroxidation, in environmental-induced neurotoxicity. While apoptosis has historically been recognized as a primary mechanism in neurotoxic events, recent evidence suggests the involvement of additional pathways, including ferroptosis. The study aims to conduct a comprehensive review of the existing literature on ferroptosis induced by environmental neurotoxicity across diverse agents such as natural toxins, insecticides, particulate matter, acrylamide, nanoparticles, plastic materials, metal overload, viral infections, anesthetics, chemotherapy, and radiation. The primary objective is to elucidate the diverse mechanisms through which these agents trigger ferroptosis, leading to neuronal cell death. Furthermore, the article explores potential preventive or therapeutic strategies that could mitigate ferroptosis, offering insights into protective measures against neurological damage induced by environmental stressors. This comprehensive review contributes to our evolving understanding of neurotoxicological processes, highlighting ferroptosis as a significant contributor to neuronal cell demise induced by environmental exposures. The insights gained from this study may pave the way for the development of targeted interventions to protect against ferroptosis-mediated neurotoxicity and ultimately safeguard public health.

摘要

神经毒性源于暴露于各种化学、生物和物理因子,对人类神经系统的复杂网络构成了重大威胁。本文探讨了铁死亡这一受调控的程序性细胞死亡形式在环境诱导的神经毒性中的作用。虽然细胞凋亡一直被认为是神经毒性事件中的主要机制,但最近的证据表明,还涉及其他途径,包括铁死亡。本研究旨在对不同环境神经毒性因子(如天然毒素、杀虫剂、颗粒物、丙烯酰胺、纳米颗粒、塑料材料、金属过载、病毒感染、麻醉剂、化疗和辐射)诱导的铁死亡相关文献进行全面综述。主要目标是阐明这些因子触发铁死亡导致神经元细胞死亡的多种机制。此外,本文还探讨了潜在的预防或治疗策略,以减轻铁死亡,为应对环境应激引起的神经损伤提供保护措施的见解。这项全面的综述有助于我们不断加深对神经毒理学过程的理解,强调铁死亡是环境暴露引起神经元细胞死亡的重要因素。本研究的结果为开发针对铁死亡介导的神经毒性的靶向干预措施提供了思路,最终保护公众健康。

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MGST1 Inhibits Sevoflurane-Induced Ferroptosis and Activates the Wnt Pathway in HT22 Cells.MGST1抑制七氟醚诱导的铁死亡并激活HT22细胞中的Wnt信号通路。
Mol Neurobiol. 2025 Mar 22. doi: 10.1007/s12035-025-04841-5.
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Polybrominated biphenyls induce liver injury by disrupting the KEAP1/Nrf2/SLC7A11 axis leading to impaired GSH synthesis and ferroptosis in hepatocytes.
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Ferroptosis induced by environmental pollutants and its health implications.环境污染物诱导的铁死亡及其对健康的影响。
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Acrylamide Induces Antiapoptotic Autophagy and Apoptosis by Activating PERK Pathway in SH-SY5Y Cells.丙烯酰胺通过激活SH-SY5Y细胞中的PERK通路诱导抗凋亡自噬和凋亡。
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