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Review
. 2014 Sep;19(5):180-9.
doi: 10.1179/1351000214Y.0000000094. Epub 2014 Apr 28.

The role of reactive oxygen species and oxidative stress in carbon monoxide toxicity: an in-depth analysis

Sumeyya Akyol, Serpil Erdogan, Nuri Idiz, Safa Celik, Mehmet Kaya, Fatma Ucar, Senol Dane, Omer Akyol
Review

The role of reactive oxygen species and oxidative stress in carbon monoxide toxicity: an in-depth analysis

Sumeyya Akyol et al. Redox Rep. 2014 Sep.

Abstract

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.

Keywords: Carbon monoxide; Free radicals; Oxidative damage; Reactive oxygen species; Toxicity.

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Figures

Figure 1.
Figure 1.
Schematic representation of the relationships among free oxygen radical formation, enzymatic antioxidant systems, and lipid peroxidation. O2−, superoxide anion radical; O2, molecular oxygen; H+, hydrogen ion, proton; H2O, water; SOD, superoxide dismutase; CAT, catalase; H2O2, hydrogen peroxide; GSH-Px, glutathione reductase; GSH, reduced glutathione; GSSG, oxidized glutathione; GSH-Red, glutathione reductase; NADPH + H+, reduced nicotinamide adenine dinucleotide phosphate; NADP+, oxidized nicotinamide adenine dinucleotide phosphate; Fe++, ferrous iron; OH−, hydroxyl ion; .OH, hydroxyl radical (the most potent free radical); tNOS, total nitric oxide synthases (neuronal NOS, endothelial NOS, and inducible NOS); NO., nitric oxide radical; ONOO−, peroxynitrite; MDA, malondialdehyde (the last product of lipid peroxidation of membrane phospholipids); NO2, nitrite; PUFA, polyunsaturated fatty acid; XO, xanthine oxidase.
Figure 2.
Figure 2.
Intrinsic CO production during heme catabolism in the body.
Figure 3.
Figure 3.
The proposed toxic effect of CO in the electron transport chain of mitochondria connected with oxidative stress.
See this image and copyright information in PMC

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