Hydrogen sulfide as an effective and specific novel therapy for acute carbon monoxide poisoning

• Published in: Biochemical and biophysical research communications 2011-01, Vol.404 (1), p.6-9
• Main Authors: Yu, Yong-Peng, Li, Zhen-Guang, Wang, Dao-Zhen, Zhan, Xia, Shao, Jing-Hua
• Format: Article
• Language: English
• Subjects: Antioxidants; Antioxidants - therapeutic use; Apoptosis; Beta cells; Carbon monoxide; Carbon Monoxide Poisoning - drug therapy; Carboxyhemoglobin; cardiomyocytes; Central nervous system; Free radicals; Humans; Hydrogen sulfide; Hydrogen Sulfide - therapeutic use; Hyperbaric oxygen; Inflammation; Lipopolysaccharides; Microglia; Necrosis; Neuromodulation; Neurons; Neuroprotection; Nitric oxide; Oxidative stress; Pancreas; Poisoning; Reactive oxygen species
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2010.11.113

► Oxidative stress, neuronal apoptosis and necrosis occur over hours to days following carbon monoxide poisoning. ► Previous studies have shown that free radical scavengers can display neuroprotective properties. ► Hydrogen sulfide (H2S) could protects neurons against oxidative stress, attenuates lipopolysaccharides (LPS) induced neuroinflammation in microglia, exhibited anti-inflammatory and anti-apoptotic activities. ► We hypothesize that H2S might be an interesting potential strategy for curing acute carbon monoxide poisoning. Hydrogen sulfide (H2S) has been recognized as a toxic gas and environment pollutant. So, it is seldom regarded as a therapeutic gas. H2S has been recognized recently as a novel gaseous messenger and serves as an important neuromodulator in the central nervous system. Many researches have been focused on the protective role of H2S in treatment of several diseases. Like nitric oxide (NO) and carbon monoxide (CO), which are considered as two gaseous transmitters, H2S has been regarded as the third one. Recent studies provided evidence that H2S exerted antioxidant and anti-apoptotic effects, which protected neurons, cardiomyocytes, pancreatic β-cells and vascular smooth muscle cells against oxidative stress by scavenging reactive oxygen species (ROS) and reactive nitrogen species (RNS). It has been known that multiple factors, including oxidative stress, free radicals and neuronal nitric oxide syntheses as well as abnormal inflammatory responses are involved in the mechanism underlying the brain injury after acute CO poisoning. Studies have shown that free radical scavengers can display neuroprotective properties. Therefore, we hypothesize that H2S might be an interesting potential strategy for curing acute CO poisoning.