# A novel yeast-derived aldehyde-reducing compound MF001 protects against alcohol-induced liver damage

**Authors:** Eun-Ho Lee, Min-Hee Seo, Soo-Young Park, Sulagna Mukherjee, Jae-Ho Lee, Sora Kang, Ji-Yu Lee, Namgyu Lee, Hung Taeck Kwon, Seung-Soon Im

PMC · DOI: 10.1371/journal.pone.0327648 · PLOS One · 2025-07-10

## TL;DR

A new compound from yeast, MF001, protects the liver from alcohol damage by reducing fat, inflammation, and oxidative stress.

## Contribution

MF001, a novel yeast-derived aldehyde-reducing compound, is introduced as a potential treatment for alcohol-induced liver damage.

## Key findings

- MF001 reduced lipid accumulation and expression of lipogenic genes in alcohol-induced liver damage.
- MF001 suppressed oxidative stress and inflammation by lowering ROS and inflammatory markers like Tnf-α, Il-6, and Mcp-1.
- MF001 modulated alcohol metabolism by downregulating Cyp2e1 and Adh1, improving liver function as shown by normalized ALT and AST levels.

## Abstract

Alcohol-induced fatty liver disease is a significant contributor to global mortality, primarily resulting from excessive alcohol consumption and subsequent hepatic damage. This study investigated the therapeutic potential of MF001, an aldehyde-reducing compound derived from the yeast Saccharomyces cerevisiae in alcohol-induced liver damage. Using a Lieber-DeCarli ethanol diet-induced live disease model, we assessed the effects of MF001 on lipogenesis, oxidative stress, and inflammation. MF001 treatment significantly reduced lipid accumulation, as indicated by decreased expression of lipogenic genes. Moreover, MF001 suppresses reactive oxygen species (ROS) production indicated by reduced malondialdehyde levels and ROS-associated inflammatory markers, including Tnf-α, Il-6, and Mcp-1. Histological analysis revealed decreased hepatic lipid deposition and inflammation following MF001 administration. Furthermore, MF001 modulated alcohol metabolism by downregulating Cyp2e1 and Adh1, thereby decreasing acetaldehyde accumulation and improving liver function, as evidenced by normalized ALT and AST levels. Our findings suggest that MF001 alleviates alcohol-induced liver damage through its anti-inflammatory, antioxidant, and lipid-lowering properties, highlighting its potential as a function agent for preventing and treating alcohol-induced fatty liver disease.

## Linked entities

- **Genes:** CYP2E1 (cytochrome P450 family 2 subfamily E member 1) [NCBI Gene 1571], ADH1A (alcohol dehydrogenase 1A (class I), alpha polypeptide) [NCBI Gene 124], TNF (tumor necrosis factor) [NCBI Gene 7124], IL6 (interleukin 6) [NCBI Gene 3569], CCL2 (C-C motif chemokine ligand 2) [NCBI Gene 6347]
- **Species:** Saccharomyces cerevisiae (taxon 4932)

## Full-text entities

- **Genes:** ADH1 (alcohol dehydrogenase ADH1) [NCBI Gene 854068] {aka ADC1}, MCP1 (Mcp1p) [NCBI Gene 854403]
- **Diseases:** fatty liver disease (MESH:D005234), inflammation (MESH:D007249), hepatic damage (MESH:D056486)
- **Chemicals:** aldehyde (MESH:D000447), malondialdehyde (MESH:D008315), MF001 (-), lipid (MESH:D008055), ROS (MESH:D017382), Alcohol (MESH:D000438), ethanol (MESH:D000431), acetaldehyde (MESH:D000079)
- **Species:** Saccharomyces cerevisiae (baker's yeast, species) [taxon 4932]

## Full text

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## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12244695/full.md

## References

41 references — full list in the complete paper: https://tomesphere.com/paper/PMC12244695/full.md

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Source: https://tomesphere.com/paper/PMC12244695