日本語フィールド
著者：Matsumoto A, Kawamoto T, Mutoh F, Isse T, Oyama T, Kitagawa K, Nakayama KI, Ichiba M.題名：Effects of 5-week ethanol feeding on the liver of aldehyde dehydrogenase 2 knockout mice.発表情報：Pharmacogenet Genomics. 巻: 18 号: 10 ページ: 847-852キーワード：acetaldehyde, alanine aminotransferase, aldehyde
dehydrogenase, ethanol, extracellular signal-regulated kinases,
knockout mice, polymorphism, tumor necrosis factor-alpha概要：抄録：Objective: The polymorphism of aldehyde dehydrogenase
2 (ALDH2), denoted ALDH2*2, is very common in East
Asian countries, and the mutated ALDH2 protein derived
from ALDH2*2 lacks the ability of acetaldehyde metabolization.
Our aim was to determine the consequences of the
ALDH2 polymorphism on ethanol-administered liver tissue.
Methods: Aldh2 + /+ , +/–, and –/– mice were fed with
ethanol solution and standard hard feed for 5 weeks.
Results: The serum alanine aminotransferase (ALT) level
in the Aldh2 – / – mice clearly decreased upon ethanol
feeding, in contrast to Aldh2 + /+ mice, in which the ALT
level was unchanged. The levels of malondialdehyde,
phospho extracellular signal-regulated kinase 2, and tumor
necrosis factor-alpha in the liver tissue all correlated with
the ALT level.
Conclusion: These findings suggest that ethanol intake in
the presence of inactive ALDH2 decreases the serum ALT
level following a decrease in oxidative stress and tumor
necrosis factor-alpha secretion.英語フィールド
Author：Matsumoto A, Kawamoto T, Mutoh F, Isse T, Oyama T, Kitagawa K, Nakayama KI, Ichiba M.Title：Effects of 5-week ethanol feeding on the liver of aldehyde dehydrogenase 2 knockout mice.Announcement information:Pharmacogenet Genomics. Vol: 18 Issue: 10 Page: 847-852Keyword：acetaldehyde, alanine aminotransferase, aldehyde
dehydrogenase, ethanol, extracellular signal-regulated kinases,
knockout mice, polymorphism, tumor necrosis factor-alphaAn abstract：Objective: The polymorphism of aldehyde dehydrogenase
2 (ALDH2), denoted ALDH2*2, is very common in East
Asian countries, and the mutated ALDH2 protein derived
from ALDH2*2 lacks the ability of acetaldehyde metabolization.
Our aim was to determine the consequences of the
ALDH2 polymorphism on ethanol-administered liver tissue.
Methods: Aldh2 + /+ , +/–, and –/– mice were fed with
ethanol solution and standard hard feed for 5 weeks.
Results: The serum alanine aminotransferase (ALT) level
in the Aldh2 – / – mice clearly decreased upon ethanol
feeding, in contrast to Aldh2 + /+ mice, in which the ALT
level was unchanged. The levels of malondialdehyde,
phospho extracellular signal-regulated kinase 2, and tumor
necrosis factor-alpha in the liver tissue all correlated with
the ALT level.
Conclusion: These findings suggest that ethanol intake in
the presence of inactive ALDH2 decreases the serum ALT
level following a decrease in oxidative stress and tumor
necrosis factor-alpha secretion.