| First Author | Matsumoto A | Year | 2016 |
| Journal | Alcohol | Volume | 52 |
| Pages | 49-54 | PubMed ID | 27139237 |
| Mgi Jnum | J:311006 | Mgi Id | MGI:6764878 |
| Doi | 10.1016/j.alcohol.2016.02.004 | Citation | Matsumoto A, et al. (2016) Heme oxygenase 1 protects ethanol-administered liver tissue in Aldh2 knockout mice. Alcohol 52:49-54 |
| abstractText | 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-alpha) 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 ALDH2*2. Our continued studies support the epidemiological finding that possession of ALDH2*2 is a protective factor in the liver of the healthy individual. |
