Alcoholic Metabolic Activation in Mice: The Role of A Small Cluster Mineral Water

Abstract To explore the molecular mechanisms underlying the effects of a specific small cluster mineral water (C-cell mineral water) on ethanol metabolism, we conducted a series of assessments comprising anti-acute alcohol toxicity experiments including behavioral hangover responses, serum ethanol levels, liver activities of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), along with metabolomic and transcriptomic analyses within 24h, and anti-chronic alcohol toxicity experiments including analysis of liver catalase (CAT) activity, along with metabolomic and transcriptomic profiling after 21d intervention of ethanol accompany with C-cell mineral water. The results suggested that the C-cell mineral water significantly delayed the latency of drunken and decreased the duration of drunken in mice, simultaneously reduced serum ethanol level at 3h and 4h. It also enhanced liver ADH and ALDH activities at 2h and activated CAT activity at 21d, compared to purified water. Transcriptomic analysis revealed that some genes related to ethanol metabolism including CYP450s, ALDH3B3, and SULT5A1 were up-regulated. Additionally, the metabolomic analysis identified that the most significantly altered pathways included primary bile acid biosynthesis, various drug metabolism pathways, and CYP450-mediated drug metabolism. Subnetworks with maximum changes featured interactions between pathways of oxidative phosphorylation, arginine biosynthesis, and primary bile acid biosynthesis, etc. The results showed that the effect of C-cell mineral water was better than that of purified water on relieving drunken, which could accelerate the conversion of acetaldehyde to acetate, and ultimately metabolize into CO₂ and H₂O through TCA cycle. These findings will provide innovative strategies for preventing acute alcoholism and relieving chronic alcohol toxicity.