Carbon monoxide (CO) poisoning remains one of the important causes of poisoning-related
deaths and acute or delayed neurological complications are still major problems (its
incidence has been reported as nearly 3–40%) for survivor-patients after CO poisoning
[
[1]
]. Although we have sufficient amount of information about reasons of brain injury
due to acute CO poisoning at gross and microscopically level, our knowledge of pathophysiological
changes at tissue level was limited until recently [
[2]
]. Recently studies have been showed that oxidative stress due to acute CO poisoning
causes overproduction of reactive oxygen species (ROS) and finally direct cellular
injury [
3
,
4
,
5
]. Therefore, today, it has been considered that inflammation, white matter demyelination,
lipid peroxidation, cytotoxic/vasogenic edema, apoptosis, and finally necrosis are
responsible for pathogenesis of brain injury due to CO poisoning [
4
,
5
,
6
].To read this article in full you will need to make a payment
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References
- Hyperbaric oxygen therapy for carbon monoxide poisoning.Undersea Hyperb. Med. 2014; 41: 339-354
- Carbon monoxide pollution and neurodevelopment: a public health concern.Neurotoxicol. Teratol. 2015; 49: 31-40
- Clinical practice. Carbon monoxide poisoning.N. Engl. J. Med. 2009; 360: 1217-1225
- Lipid peroxidation was involved in the memory impairment of carbon monoxide-induced delayed neuron damage.Neurochem. Res. 2009; 34: 1293-1298
- Induction of heme oxygenase-1 with hemin attenuates hippocampal injury in rats after acute carbon monoxide poisoning.Toxicology. 2009; 262: 146-152
- Xanthine oxidoreductase and neurological sequelae of carbon monoxide poisoning.Toxicol. Lett. 2007; 170: 111-115
- G-CSF administration attenuates brain injury in rats following carbon monoxide poisoning via different mechanisms.Environ. Toxicol. 2015; https://doi.org/10.1002/tox.22210
- Erythropoietin protects rat brain injury from carbon monoxide poisoning by inhibiting toll-like receptor 4/NF-kappa B-dependent inflammatory responses.Inflammation. 2016; 39: 561-568
- Allopurinol reduces severity of delayed neurologic sequelae in experimental carbon monoxide toxicity in rats.Neurotoxicology. 2015; 48: 171-179
- Neuroprotective effect of hydrogen-rich saline in acute carbon monoxide poisoning.CNS Neurosci Ther. 2013; 19: 361-363
- Neuroprotective effects of methane-rich saline on experimental acute carbon monoxide toxicity.J. Neurol. Sci. 2016; 369: 361-367
- Methane attenuates hepatic ischemia-reperfusion injury in rats through anti-apoptosis, anti-inflammatory and anti-oxidative.Shock. 2015; 44: 181-187
- Methane attenuates myocardial ischemia injury in rats through anti-oxidative, anti-apoptotic and anti-inflammatory actions.Free Radic. Biol. Med. 2016; 90: 1-11
Article info
Publication history
Published online: August 28, 2016
Accepted:
August 24,
2016
Received:
August 22,
2016
Identification
Copyright
© 2016 Elsevier B.V. All rights reserved.
