Hydrogen Gas Protects Brain from Carbon Monoxide Poisoning
- Authors
- Meihua Shen, Yijun Zheng, Kaimin Zhu, Zhonghai Cai, Wenwu Liu, Xuejun Sun, Jiankang Liu, Duming Zhu
- Journal
- Neurological Research
- Year
- 2019
- DOI
- 10.1080/01616412.2019.1685064
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Carbon Monoxide Poisoning
- Body System
- Nervous System
TL;DR
Breathing high concentrations of hydrogen gas can significantly reduce brain damage and improve recovery after carbon monoxide poisoning in rats.
Key Finding
High-concentration hydrogen gas (67% H2) significantly reduced neurological damage and oxidative stress markers in rats with delayed brain complications from carbon monoxide poisoning, with effects mediated through activation of the Nrf2 antioxidant pathway.
Summary
This rat study tested whether high-concentration hydrogen gas (67% hydrogen mixed with oxygen) could protect the brain from damage caused by carbon monoxide poisoning. Rats exposed to carbon monoxide showed neurological problems, but those treated with hydrogen gas for 90 minutes after poisoning showed significant improvement in brain function and had lower levels of harmful molecules (oxidative stress markers) in their blood and brain tissue.
Practical Takeaway
While this rat study suggests hydrogen gas may have protective effects against carbon monoxide poisoning complications, it is a preliminary animal study and cannot be directly applied to humans. Any potential clinical use would require human trials to establish safety and effectiveness. This research does not support self-treatment with hydrogen gas for carbon monoxide exposure.
Abstract
Objective: The protective effects of 2%-4% hydrogen gas in delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) have been previously reported. This study aimed to assess the neuroprotective effects of high concentration hydrogen (HCH) on DEACMP. Methods: A total of 36 male Sprague-Dawley rats were divided into 3 groups. In the DEACMP group, rats were exposed to CO to induce CO poisoning; in the HCH group, the animals were exposed to 67% H2 and 33% O2 at 3,000 mL/min for 90 min immediately after CO poisoning. Neurological function was evaluated at 1 and 9 days after poisoning. Then, the contents of malondialdehyde, 3-nitrotyrosine and 8-hydroxy-2-deoxyguanosine, as well as superoxide dismutase activity in the serum, cortex and hippocampus were detected by ELISA. Additionally, the mRNA and protein expression levels of Nrf2 and downstream genes were detected by RT-PCR and Western blotting, respectively. Results: Our results showed that CO poisoning significantly impaired neurological function which was improved over time, and HCH markedly attenuated neurological impairment following CO poisoning. In addition, CO poisoning resulted in increased levels of malondialdehyde, 3-nitrotyrosine and 8-hydroxy-2-deoxyguanosine and markedly reduced superoxide dismutase activity at 1 and 9 days, which were significantly inhibited by HCH at 9 days. Finally, CO poisoning increased the mRNA and protein levels of Nrf2 and downstream genes, and HCH further induced the anti-oxidative capability. Conclusion: These findings indicate the neuroprotective effects of HCH on DEACMP, which are related to the activation of Nrf2 signaling pathway.