ArticleFrontiers in pharmacology2026
Restoring redox homeostasis through S-adenosyl-L-methionine and B-vitamins co-supplementation alleviates ethanol induced hepato-pancreatic injury by regulating glutathione biosynthesis in C57BL/6J mice.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Vitamins as modulators of Deltaretrovirus infection: implications for HTLV-1 and bovine leukemia virus-associated diseases.Archives of microbiology · 2026Review
- Systems-level identification of conserved molecular drivers underlying the progression of alcoholic hepatitis and alcoholic cirrhosis and their therapeutic modulation by S-adenosyl-L-methionine.Frontiers in bioinformatics · 2026Article
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Authors and funding
2 authors.
Funding
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Abstract
Background: Alcohol use disorder(AUD) is a chronic condition responsible for more than 3 million deaths annually worldwide and contributes to the development of multiple systemic comorbidities. Chronic alcohol consumption promotes inflammatory responses, immune suppression, antioxidant dysregulation, and nutritional deficiencies, severely affecting organs such as the liver and pancreas. Disruption of methionine metabolism and antioxidant defenses, including reduced availability of S-adenosyl-L-methionine (SAMe) and essential B-vitamins, has been implicated in alcohol-induced oxidative stress. Therefore, the aim of the present study was to investigate whether co-supplementation with SAMe and B-vitamins could alleviate ethanol-induced hepato-pancreatic injury by improving redox homeostasis and glutathione biosynthesis. Methods: C57BL/6J male mice (n = 6 per group) were used to model acute-on-chronic alcohol-associated liver injury using the NIAAA chronic-plus-binge ethanol feeding model. From days 1-10, mice were fed a Lieber-DeCarli liquid diet containing 5% (v/v) ethanol Results: SAMe and B-vitamin co-supplementation significantly attenuated ethanol-induced hepato-pancreatic injury, evidenced by reduced activities of amylase, alanine aminotransferase, and aspartate aminotransferase, myeloperoxidase ( Conclusion: Chronic ethanol exposure induces profound oxidative stress and impairs endogenous antioxidant defence system, culminating in severe hepato-pancreatic injury. Restoration of glutathione homeostasis and stabilization of cellular redox balance through SAMe and B-vitamins co-supplementation efficiently attenuated organ pathology, thereby improving the overall wellbeing of the affected individual.
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