Abramov Andrey Y, Myers Isabella, Angelova Plamena R
UCL Queen Square Institute of Neurology, Department of Clinical and Movement Neurosciences, Queen Square, London WC1N3BG, UK.
Antioxidants (Basel). 2024 Sep 16;13(9):1121. doi: 10.3390/antiox13091121.
Despite recent technological progress, carbon monoxide poisoning is still one of the leading causes of domestic and industrial morbidity and mortality. The brain is particularly vulnerable to CO toxicity, and thus the majority of survivors develop delayed movement and cognitive complications. CO binds to haemoglobin in erythrocytes, preventing oxygen delivery to tissues, and additionally inhibits mitochondrial respiration. This renders the effect of CO to be closely related to hypoxia reperfusion injury. Oxygen deprivation, as well as CO poisoning and re-oxygenation, are shown to be able to activate the production of reactive oxygen species and to induce oxidative stress. Here, we review the role of reactive oxygen species production and oxidative stress in the mechanism of neuronal cell death induced by carbon monoxide and re-oxygenation. We discuss possible protective mechanisms used by brain cells with a specific focus on the inhibition of CO-induced ROS production and oxidative stress.
尽管最近技术有所进步，但一氧化碳中毒仍然是家庭和工业发病及死亡的主要原因之一。大脑对一氧化碳毒性尤为敏感，因此大多数幸存者会出现迟发性运动和认知并发症。一氧化碳与红细胞中的血红蛋白结合，阻止氧气输送到组织，此外还抑制线粒体呼吸。这使得一氧化碳的作用与缺氧再灌注损伤密切相关。缺氧以及一氧化碳中毒和再给氧均显示能够激活活性氧的产生并诱导氧化应激。在此，我们综述活性氧产生和氧化应激在一氧化碳和再给氧诱导的神经元细胞死亡机制中的作用。我们讨论脑细胞可能采用的保护机制，特别关注抑制一氧化碳诱导的活性氧产生和氧化应激。
