Akyol Sumeyya, Erdogan Serpil, Idiz Nuri, Celik Safa, Kaya Mehmet, Ucar Fatma, Dane Senol, Akyol Omer
Redox Rep. 2014 Sep;19(5):180-9. doi: 10.1179/1351000214Y.0000000094. Epub 2014 Apr 28.
The underlying mechanism of the central nervous system (CNS) injury after acute carbon monoxide (CO) poisoning is interlaced with multiple factors including apoptosis, abnormal inflammatory responses, hypoxia, and ischemia/reperfusion-like problems. One of the current hypotheses with regard to the molecular mechanism of CO poisoning is the oxidative injury induced by reactive oxygen species, free radicals, and neuronal nitric oxide. Up to now, the relevant mechanism of this injury remains poorly understood. The weakening of antioxidant systems and the increase of lipid peroxidation in the CNS have been implicated, however. Accordingly, in this review, we will highlight the relationship between oxidative stress and CO poisoning from the perspective of forensic toxicology and molecular toxicology.
急性一氧化碳（CO）中毒后中枢神经系统（CNS）损伤的潜在机制与多种因素交织在一起，包括细胞凋亡、异常炎症反应、缺氧以及缺血/再灌注样问题。目前关于CO中毒分子机制的假说之一是活性氧、自由基和神经元一氧化氮诱导的氧化损伤。到目前为止，这种损伤的相关机制仍知之甚少。然而，中枢神经系统中抗氧化系统的减弱和脂质过氧化的增加已被牵连其中。因此，在本综述中，我们将从法医毒理学和分子毒理学的角度突出氧化应激与CO中毒之间的关系。
