ArticleMolecular biology reports2026
Molecular and toxicogenetic safety profile of short-term nitrous oxide anesthesia in surgical patients.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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7 authors.
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Abstract
backgroundNitrous oxide (N2O) is a widely used anesthetic; however, its potential to compromise genomic stability by disrupting vitamin B12 and folate metabolism remains a critical concern in clinical molecular biology. Since N2O can oxidize cobalamin, it may theoretically impair the methionine synthase pathway, leading to DNA damage. Thus, this study aimed to evaluate the toxicogenetic impact-DNA damage and gene expression-and the metabolic profile of vitamins B9 and B12, homocysteine (HCY) and micronutrients/antioxidants in patients undergoing short-term N2O anesthesia. METHODS AND
resultsAdult surgical patients without comorbidities (n = 18/group) were assessed at: pre-anesthesia, during anesthesia (1.5 h exposure), and 24 h post-anesthesia. Both groups received desflurane, with one also receiving N2O. The primary focus was on DNA strand breaks (comet assay) and the transcriptional levels (RT-qPCR) of repair (OGG1 and XRCC1) and antioxidant (HO-1) genes, followed by HPLC and chemiluminescence analysis of metabolic markers (HCY and antioxidants, vitamins B9 and B12). N2O exposure did not modulate the mRNA expression of any of the studied genes, nor did it alter HCY, vitamin levels or antioxidants (p > 0.05). A transient, group-independent increase in DNA damage was observed post-anesthesia, suggesting a primary response to surgical stress rather than the anesthetic agent.
conclusionsOur study provides high-evidence molecular data demonstrating that 1.5 h of N2O exposure is safe for genomic integrity and vitamin B-related metabolism in healthy individuals. These findings are clinically relevant as they validate the continued use of N2O in minimally invasive procedures without the risk of acute toxicogenetic or metabolic impairment.
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