Onions may be effective in mitigating hangover symptoms and reducing the risk of alcoholic liver disease. A research group led by Professor Yoshimasa Nakamura and Associate Professor Toshiyuki Nakamura of the Graduate School of Environmental, Life, Natural Science and Technology, and Associate Professor Ayano Satoh of the Graduate School of Interdisciplinary Science and Engineering in Health Systems at Okayama University, has used hepatocyte models of ALDH2 genetic polymorphism-dependent alcohol intolerance, which is unique to East Asian people, to elucidate the protective effect of a polyphenol (quercetin), which is abundant in onions and other plants, against acetaldehyde toxicity and the underlying molecular mechanism. Furthermore, quercetin protects cells from acetaldehyde toxicity through its ability to enhance the expression of antioxidant-producing enzymes as well as acetaldehyde-metabolizing enzymes.
The research results on the functionality of the food component and its molecular mechanisms revealed in this study provide a new scientific basis for the health-promoting effects of polyphenols. They are expected to contribute significantly to the scientific understanding of food functionality and safety. The findings are also expected to contribute to the development of new functional foods and dietary supplements based on the cytoprotective action of quercetin against acetaldehyde toxicity.
The results were published in Bioscience, Biotechnology, and Biochemistry, an international scientific journal of the Japan Society for Bioscience, Biotechnology, and Agrochemistry, and the International Journal of Molecular Sciences in Switzerland.
Journal Information
Publication: Bioscience, Biotechnology, and Biochemistry
Title: Evaluation of quercetin as a potential cytoprotector against acetaldehyde using the cultured hepatocyte model with aldehyde dehydrogenase isozyme deficiency
DOI: 10.1093/bbb/zbae100
Publication: International Journal of Molecular Sciences
Title: Quercetin Attenuates Acetaldehyde-Induced Cytotoxicity via the Heme Oxygenase-1-Dependent Antioxidant Mechanism in Hepatocytes
DOI: 10.3390/ijms25169038
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