Neurotoxicology · 2025
Toxicological effects of diquat on the central nervous system and associated treatment challenges.
СтатьяСистематический обзорНазвание и аннотация: Перевод в очереди
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Wang Xinyu, Liu Yunxia, Yang Meng, Wang Yunwen, Guo Feng, Wang Lin
Аннотация
BACKGROUND: Diquat is a highly toxic pyridine-based herbicide, and its central nervous system (CNS) toxicity is a major factor contributing to the high mortality rate and poor neurological outcomes in poisoned patients. Compared with other organ injuries, the complex molecular mechanisms underlying diquat-induced CNS damage and effective neuroprotective strategies remain poorly understood.
METHODS: A systematic search and screening of relevant literature on diquat-induced CNS toxicity were conducted. Based on predefined inclusion and exclusion criteria, 21 articles were selected from 424 retrieved records, including 11 experimental and 10 case studies. A systematic review approach was employed to integrate basic research with clinical evidence.
RESULTS: The study identified typical clinical manifestations of CNS damage caused by diquat poisoning (e.g., impaired consciousness, convulsions, and brainstem symptoms), along with characteristic imaging findings (e.g., lesions in the basal ganglia and brainstem). The core findings highlight six major mechanisms underlying diquat-induced neural damage: excessive activation of the oxidative stress response; pronounced neuroinflammatory cascade reactions; dysregulated autophagy function; activation of apoptotic signaling pathways; mitochondrial dysfunction; and significant alterations in the neurotransmitter system. These mechanisms are interrelated and collectively lead to neuronal death and functional impairment.
CONCLUSIONS: Diquat induces severe CNS damage through multiple interrelated molecular mechanisms. Current diagnostic and therapeutic strategies face significant challenges in improving neurological outcomes, particularly due to the lack of specific antidotes and targeted neuroprotective agents. Future research should aim to elucidate the underlying mechanisms in detail, explore novel neuroprotective targets, optimize comprehensive treatment protocols, and develop long-term rehabilitation strategies to reduce neurological impairment and mortality associated with diquat poisoning.
METHODS: A systematic search and screening of relevant literature on diquat-induced CNS toxicity were conducted. Based on predefined inclusion and exclusion criteria, 21 articles were selected from 424 retrieved records, including 11 experimental and 10 case studies. A systematic review approach was employed to integrate basic research with clinical evidence.
RESULTS: The study identified typical clinical manifestations of CNS damage caused by diquat poisoning (e.g., impaired consciousness, convulsions, and brainstem symptoms), along with characteristic imaging findings (e.g., lesions in the basal ganglia and brainstem). The core findings highlight six major mechanisms underlying diquat-induced neural damage: excessive activation of the oxidative stress response; pronounced neuroinflammatory cascade reactions; dysregulated autophagy function; activation of apoptotic signaling pathways; mitochondrial dysfunction; and significant alterations in the neurotransmitter system. These mechanisms are interrelated and collectively lead to neuronal death and functional impairment.
CONCLUSIONS: Diquat induces severe CNS damage through multiple interrelated molecular mechanisms. Current diagnostic and therapeutic strategies face significant challenges in improving neurological outcomes, particularly due to the lack of specific antidotes and targeted neuroprotective agents. Future research should aim to elucidate the underlying mechanisms in detail, explore novel neuroprotective targets, optimize comprehensive treatment protocols, and develop long-term rehabilitation strategies to reduce neurological impairment and mortality associated with diquat poisoning.