Hydrogen Saline Protects Brain from Carbon Monoxide Poisoning in Rats
- Authors
- Wenlan Wang, Liang Tian, Ya Li, Xiaojun Wang, Feng Xia, Li Li, Jinsheng Li, Zuo-Ming Zhang
- Journal
- The Journal of Emergency Medicine
- Year
- 2013
- DOI
- 10.1016/j.jemermed.2012.01.065
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Carbon Monoxide Poisoning
- Body System
- Nervous System
TL;DR
A special saline solution rich in hydrogen gas can reduce brain damage in rats poisoned with carbon monoxide.
Key Finding
Hydrogen-rich saline improved cognitive function and reduced brain cell death in rats with acute carbon monoxide poisoning, possibly by reducing oxidative damage and altering trace element levels.
Summary
Researchers gave rats poisoned with carbon monoxide either hydrogen-rich saline or a control treatment. Carbon monoxide damages the brain partly by creating harmful molecules called free radicals. Hydrogen acts as an antioxidant (a substance that neutralizes free radicals). Rats treated with hydrogen-rich saline showed better memory and learning, less brain cell death, and changes in trace metals (copper and iron) associated with reduced oxidative damage compared to untreated rats.
Practical Takeaway
This is an early-stage animal study showing hydrogen-rich saline may protect against carbon monoxide poisoning damage in rats. However, results from animal studies do not automatically translate to humans, and no human trials have tested this approach. Much more research would be needed before any clinical application could be considered.
Abstract
Background: Studies have shown that inhalation of hydrogen gas, which acts as an antioxidant, can protect the brain against free radicals in rats with ischemia-reperfusion. The neuronal damage caused by acute carbon monoxide (CO) poisoning is partly free radical mediated. We hypothesize that hydrogen may prevent neurological damage from CO poisoning. Objectives: This study is designed to test whether hydrogen (H(2))-rich saline will have a protective effect on rats with acute CO poisoning. Methods: Male Sprague-Dawley rats were subjected to CO poisoning. H(2)-rich saline was administered by peritoneal injection (6 mL/kg/24 h). We used the Morris water maze and the open field test to determine cognitive function. After cognitive function studies, rats were decapitated and the levels of trace elements copper (Cu), zinc (Zn), and iron (Fe) in serum and brain were assessed by flame atomic absorption spectrometry. Necrosis, apoptosis, and autophagy of neurons were assessed by H-E staining and immunohistochemical staining in another group of rats. Results: H(2)-rich saline treatment improved the cognitive deficits and reduced the degree of necrosis, apoptosis, and cell autophagy in rats. Additionally, H(2)-rich saline decreased the content of Fe in serum and brain in these rats, and increased the content of serum Cu related to free radical metabolism. Conclusions: H(2)-rich saline may effectively protect the brain from injury after acute CO poisoning. The mechanism of this protection may be related to lessening oxidative damage by affecting trace elements in vivo.