Hydrogen Gas Protects Newborn Brains from Anesthesia-Related Damage
- Authors
- Masumi Iketani, Mai Hatomi, Yasunori Fujita, Nobuhiro Watanabe, Masafumi Ito, Hideo Kawaguchi, Ikuroh Ohsawa
- Journal
- Journal of Neurochemistry
- Year
- 2024
- DOI
- 10.1111/jnc.16142
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Anesthesia-Induced Neurotoxicity
- Body System
- Nervous System
TL;DR
Breathing in hydrogen gas can protect newborn mice's brains from damage caused by a common anesthesia gas.
Key Finding
Hydrogen gas inhalation reduced sevoflurane-induced brain cell death in newborn mice by suppressing cell death pathways and decreasing oxidative stress markers like lipid peroxidation and DNA damage.
Summary
This study tested whether hydrogen gas could protect newborn mouse brains from damage caused by sevoflurane, a common anesthetic gas. Researchers exposed newborn mice to sevoflurane and found it triggered cell death in brain cells. When they also gave the mice hydrogen gas to breathe for 3 hours, the hydrogen reduced this cell death and decreased markers of oxidative stress (cellular damage from harmful molecules). The hydrogen appeared to work by changing how certain proteins were modified in the brain cells.
Practical Takeaway
This is an early-stage animal study in newborn mice, not humans, so it cannot yet inform clinical decisions about hydrogen water or hydrogen gas for people. While the results suggest hydrogen may have protective properties against anesthetic-induced brain injury, much more research—including human studies—would be needed before any therapeutic recommendations could be made. The study's relevance to hydrogen water consumption (rather than medical-grade hydrogen gas inhalation) remains unclear.
Abstract
Inhalation of hydrogen (H2) gas is therapeutically effective for cerebrovascular diseases, neurodegenerative disorders, and neonatal brain disorders including pathologies induced by anesthetic gases. To understand the mechanisms underlying the protective effects of H2 on the brain, we investigated the molecular signals affected by H2 in sevoflurane-induced neuronal cell death. We confirmed that neural progenitor cells are susceptible to sevoflurane and undergo apoptosis in the retrosplenial cortex of neonatal mice. Co-administration of 1-8% H2 gas for 3 h to sevoflurane-exposed pups suppressed elevated caspase-3-mediated apoptotic cell death and concomitantly decreased c-Jun phosphorylation and activation of the c-Jun pathway, all of which are induced by oxidative stress. Anesthesia-induced increases in lipid peroxidation and oxidative DNA damage were alleviated by H2 inhalation. Phosphoproteome analysis revealed enriched clusters of differentially phosphorylated proteins in the sevoflurane-exposed neonatal brain that included proteins involved in neuronal development and synaptic signaling. H2 inhalation modified cellular transport pathways that depend on hyperphosphorylated proteins including microtubule-associated protein family. These modifications may be involved in the protective mechanisms of H2 against sevoflurane-induced neuronal cell death.