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• W2292795655 abstract "A genetic polymorphism of the aldehyde dehydrogenase 2 (​ALDH2) gene, ALDH2*2, encodes an enzymatically defective ALDH2 protein. Recent epidemiological studies suggest that possessing ALDH2*2 is a protective factor for liver tissue in healthy individuals, although these studies lack a mechanistic explanation. Our animal studies have shown the same trend: levels of serum alanine transaminase (ALT), hepatic malondialdehyde (MDA), and hepatic tumor necrosis factor alpha (TNF-α) were lower in Aldh2 knockout (Aldh2−/−) mice than in wild-type (Aldh2+/+) mice after ethanol administration. To propose a mechanistic hypothesis, residual liver specimens from the previous experiment were analyzed. An anti-oxidative protein, heme oxygenase 1 (HO-1), and an oxidative stress-producing protein, cytochrome P450 2E1 (CYP2E1), were detected at higher levels in Aldh2−/− mice than in Aldh2+/+ mice, regardless of ethanol treatment. Other oxidative stress-related proteins and inflammatory cytokines did not show such a significant difference. To conclude, we propose a protective role of HO-1 in individuals with A​LDH2*2. Our continued studies support the epidemiological finding that possession of ALDH2*2 is a protective factor in the liver of the healthy individual." @default.
• W2292795655 created "2016-06-24" @default.
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• W2292795655 date "2016-05-01" @default.
• W2292795655 modified "2023-10-17" @default.
• W2292795655 title "Heme oxygenase 1 protects ethanol-administered liver tissue in Aldh2 knockout mice" @default.
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• W2292795655 doi "https://doi.org/10.1016/j.alcohol.2016.02.004" @default.
• W2292795655 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27139237" @default.
• W2292795655 hasPublicationYear "2016" @default.
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