作者: PS Haber , RT Gentry , KM Mak , SA Mirmiran-Yazdy , RJ Greenstein
DOI: 10.1016/S0016-5085(96)70054-9
关键词: Ethanol 、 Stomach 、 Metabolism 、 Ethanol metabolism 、 Internal medicine 、 Cimetidine 、 Gastric mucosa 、 First pass effect 、 Alcohol dehydrogenase 、 Biology 、 Endocrinology
摘要: BACKGROUND & AIMS: The bioavailability of orally administered alcohol is incomplete, indicating first-pass metabolism. There debate regarding the site metabolism and specifically whether stomach has metabolic capacity to account for aim this study was assess ethanol by human gastric mucosa cells in primary culture. METHODS: Cells were incubated with [1-14C]ethanol, quantity oxidized measured production [1-14C]acetate. RESULTS: Gastric cultured from men produced 7.3 +/- 3.5 mumol acetate.10(6) cells-1.h-1, which more than that generated women (3.2 0.6; P < 0.05). Acetate inhibited 4-methylpyrazole (a class I dehydrogenase [ADH] inhibitor) m-nitrobenzaldehyde selective substrate IV ADH isoenzyme) but not sodium azide catalase inhibitor). Cimetidine reduced acetate as much 59%, whereas ranitidine had no significant effect. CONCLUSIONS: Human metabolize sufficient bulk At least two isozymes contribute Cimetidine, ranitidine, inhibits keeping its inhibition vivo (Gastroenterology 1996 Oct;111(4):863-70)