Arda-Pirincci Pelin, Bilgin-Sokmen Bahar, Yanardag Refiye, Bolkent Sehnaz
Department of Biology, Faculty of Science, Istanbul University, Vezneciler, Turkey.
Biosci Biotechnol Biochem. 2009 Feb;73(2):260-7. doi: 10.1271/bbb.70805. Epub 2009 Feb 7.
This study was designed to determine the morphological and biochemical effects of zinc sulfate and the role of metallothionein in ethanol-induced intestinal injury. Rats received zinc sulfate (100 mg/kg/d) for 3 consecutive d, 2 h prior to the administration of ethanol by gavage. Ethanol administration caused intestinal injury as determined by increased serum lactate dehydrogenase activity, urea, creatinine, uric acid, and sialic acid levels, intestinal lipid peroxidation level, decreased serum catalase activity, intestinal glutathione level, and metallothionein expression. Zinc sulfate pretreatment of the ethanol group caused a decrease in histological damage, serum lactate dehydrogenase activity, urea, creatinine, uric acid, sialic acid levels, and intestinal lipid peroxidation level, but increases in serum catalase activity, intestinal glutathione level, and metallothionein expression. The present study indicates that zinc sulfate has a protective effect against ethanol-induced intestinal injury. In addition, the protective effect of zinc on ethanol-induced intestinal injury might be mediated by metallothionein, as well as having antioxidative potential.
本研究旨在确定硫酸锌的形态学和生化效应以及金属硫蛋白在乙醇诱导的肠道损伤中的作用。大鼠在通过灌胃给予乙醇前2小时,连续3天接受硫酸锌(100毫克/千克/天)。乙醇给药导致肠道损伤,这可通过血清乳酸脱氢酶活性、尿素、肌酐、尿酸和唾液酸水平升高、肠道脂质过氧化水平升高、血清过氧化氢酶活性降低、肠道谷胱甘肽水平降低以及金属硫蛋白表达降低来确定。乙醇组的硫酸锌预处理导致组织学损伤、血清乳酸脱氢酶活性、尿素、肌酐、尿酸、唾液酸水平以及肠道脂质过氧化水平降低,但血清过氧化氢酶活性、肠道谷胱甘肽水平以及金属硫蛋白表达增加。本研究表明硫酸锌对乙醇诱导的肠道损伤具有保护作用。此外,锌对乙醇诱导的肠道损伤的保护作用可能由金属硫蛋白介导,并且具有抗氧化潜力。