Degradation effects and mechanisms of Limosilactobacillus fermentum on ethanol

Abstract

Acute heavy drinking can lead to a rapid increase in blood ethanol concentration, resulting in dizziness, liver damage, and other adverse effects. Although lactic acid bacteria possess the ability to degrade ethanol, the mechanisms remain unclear. For the first time, our study revealed that Limosilactobacillus fermentum DACN611, derived from traditional Chinese fermented yogurt, exhibited superior ethanol degradation capability, achieving a 90.87% ± 8.12% reduction in ethanol concentration in a 2.5% (v/v) ethanol MRS broth over 24 h, among fifty lactic acid bacteria strains. Notably, transcriptome analysis of DACN611 under ethanol stress conditions revealed that DACN611 degraded ethanol by adjusting the cell cycle, promoting protein synthesis, maintaining oxidative metabolic homeostasis, and modulating cell wall and membrane synthesis along with other metabolic pathways. Additionally, DACN611 showed excellent resistance to gastric acid and bile salts, along with a safe profile. In the acute heavy drinking Kunming mouse model, DACN611 significantly increased the latency of the loss of righting reflex (LORR) and reduced the LORR duration. Serum ethanol and acetaldehyde concentrations decreased by 35.36% and 33.56%, respectively. The gastric and hepatic activities of alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH) increased by 1.98-fold and 1.95-fold, and 1.79-fold and 1.70-fold, respectively. In addition, DACN611 decreased serum alanine aminotransferase and aspartate aminotransferase levels, and reduced hepatic cytochrome P450 2E1 expression. It also alleviated pathological liver changes, demonstrating protective effects against alcoholic liver injury in mice. In conclusion, DACN611 significantly degraded ethanol through adaptive metabolic changes under ethanol stress conditions and the promotion of ADH and ALDH activities in gastric and hepatic tissues.