dose-dependent change in elimination kinetics of ethanol due to shift of dominant metabolizing enzyme from adh 1 (class i) to adh 3 (class iii) in mouse存在剂量依赖的相关性消除乙醇由于转变的动力学变化的主要代谢酶adh 1(一级)抗利尿激素3(第三类)的老鼠.pdfVIP

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dose-dependent change in elimination kinetics of ethanol due to shift of dominant metabolizing enzyme from adh 1 (class i) to adh 3 (class iii) in mouse存在剂量依赖的相关性消除乙醇由于转变的动力学变化的主要代谢酶adh 1(一级)抗利尿激素3(第三类)的老鼠.pdf

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dose-dependent change in elimination kinetics of ethanol due to shift of dominant metabolizing enzyme from adh 1 (class i) to adh 3 (class iii) in mouse存在剂量依赖的相关性消除乙醇由于转变的动力学变化的主要代谢酶adh 1(一级)抗利尿激素3(第三类)的老鼠

Hindawi Publishing Corporation International Journal of Hepatology Volume 2012, Article ID 408190, 8 pages doi:10.1155/2012/408190 Research Article Dose-Dependent Change in Elimination Kinetics of Ethanol due to Shift of Dominant Metabolizing Enzyme from ADH 1 (Class I) to ADH 3 (Class III) in Mouse Takeshi Haseba,1 Kouji Kameyama,2 Keiko Mashimo,1 and Youkichi Ohno1 1 Department of Legal Medicine, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan 2 Department of Pathology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan Correspondence should be addressed to Takeshi Haseba, hasebat@nms.ac.jp Received 27 May 2011; Accepted 23 August 2011 Academic Editor: Angela Dolganiuc Copyright © 2012 Takeshi Haseba et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ADH 1 and ADH 3 are major two ADH isozymes in the liver, which participate in systemic alcohol metabolism, mainly distributing in parenchymal and in sinusoidal endothelial cells of the liver, respectively. We investigated how these two ADHs contribute to the elimination kinetics of blood ethanol by administering ethanol to mice at various doses, and by measuring liver ADH activity and liver contents of both ADHs. The normalized AUC (AUC/dose) showed a concave increase with an increase in ethanol dose, inversely correlating with β . CLT (dose/AUC) linearly correlated with liver ADH activity and also with both the ADH-1 and -3 contents (mg/kg B.W.). When ADH-1 activity was calculated by multiplying ADH-1 content by its Vmax /mg (4.0) and normalized by the ratio of liver ADH activity of each ethanol dose to that of the contr