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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Yamazaki H, Nishiguchi K, Inoue K, Yasuyama T, Nakanishi S

Department of Pharmacology, Faculty of Medicine, Toyama Medical and Pharmaceutical University, Japan.

Int J Biochem. 1988;20(4):435-7. doi: 10.1016/0020-711x(88)90212-1.

The activity of liver microsomal high Km-ALDH and mitochondrial low Km-ALDH, which may be primarily responsible for the oxidation of acetaldehyde after ethanol administration was found to be predominantly distributed in the centrilobular area. 2. The activities of other ALDH isozymes in mitochondrial and soluble fractions were evenly distributed in periportal and perivenous regions. 3. The activity of ADH which is involved in production of acetaldehyde was predominantly located in the periportal area. 4. From these results it seems unlikely that a concentration of acetaldehyde after ethanol ingestion is higher in perivenous hepatocytes than in periportal ones. Additional data would be needed to understand fully the mechanism by which ethanol induces predominantly centrilobular liver injury.

Yamazaki H, Nishiguchi K, Inoue K, Yasuyama T, Nakanishi S

Department of Pharmacology, Faculty of Medicine, Toyama Medical and Pharmaceutical University, Japan.

Int J Biochem. 1988;20(4):435-7. doi: 10.1016/0020-711x(88)90212-1.

The activity of liver microsomal high Km-ALDH and mitochondrial low Km-ALDH, which may be primarily responsible for the oxidation of acetaldehyde after ethanol administration was found to be predominantly distributed in the centrilobular area. 2. The activities of other ALDH isozymes in mitochondrial and soluble fractions were evenly distributed in periportal and perivenous regions. 3. The activity of ADH which is involved in production of acetaldehyde was predominantly located in the periportal area. 4. From these results it seems unlikely that a concentration of acetaldehyde after ethanol ingestion is higher in perivenous hepatocytes than in periportal ones. Additional data would be needed to understand fully the mechanism by which ethanol induces predominantly centrilobular liver injury.