Bolkent Sema, Arda-Pirincci Pelin, Bolkent Sehnaz, Yanardag Refiye, Tunali Sevim, Yildirim Sukriye
Department of Medical Biology, Cerrahpasa Faculty of Medicine, Istanbul University, Cerrahpasa 34098, Istanbul, Turkey.
World J Gastroenterol. 2006 Jul 21;12(27):4345-51. doi: 10.3748/wjg.v12.i27.4345.
To investigate the role of metallothionein and proliferating cell nuclear antigen (PCNA) on the morphological and biochemical effects of zinc sulfate in ethanol-induced liver injury.
Wistar albino rats were divided into four groups. Group I; intact rats, group II; control rats given only zinc, group III; animals given absolute ethanol, group IV; rats given zinc and absolute ethanol. Ethanol-induced injury was produced by the 1 mL of absolute ethanol, administrated by gavage technique to each rat. Animals received 100 mg/kg per day zinc sulfate for 3 d 2 h prior to the administration of absolute ethanol.
Increases in metallothionein immunoreactivity in control rats given only zinc and rats given zinc and ethanol were observed. PCNA immunohistochemistry showed that the number of PCNA-positive hepatocytes was increased significantly in the livers of rats administered ethanol + zinc sulfate. Acute ethanol exposure caused degenerative morphological changes in the liver. Blood glutathione levels decreased, serum alkaline phosphatase and aspartate transaminase activities increased in the ethanol group when compared to the control group. Liver glutathione levels were reduced, but lipid peroxidation increased in the livers of the group administered ethanol as compared to the other groups. Administration of zinc sulfate in the ethanol group caused a significant decrease in degenerative changes, lipid peroxidation, and alkaline phosphatase and aspartate transaminase activities, but an increase in liver glutathione.
Zinc sulfate has a protective effect on ethanol-induced liver injury. In addition, cell proliferation may be related to the increase in metallothionein immunoreactivity in the livers of rats administered ethanol + zinc sulfate.
研究金属硫蛋白和增殖细胞核抗原(PCNA)在硫酸锌对乙醇诱导的肝损伤的形态学和生化作用中的作用。
将Wistar白化大鼠分为四组。第一组;完整大鼠,第二组;仅给予锌的对照大鼠,第三组;给予无水乙醇的动物,第四组;给予锌和无水乙醇的大鼠。通过灌胃技术给每只大鼠灌胃1 mL无水乙醇诱导肝损伤。在给予无水乙醇前3天2小时,动物每天接受100 mg/kg硫酸锌。
观察到仅给予锌的对照大鼠以及给予锌和乙醇的大鼠中金属硫蛋白免疫反应性增加。PCNA免疫组织化学显示,给予乙醇+硫酸锌的大鼠肝脏中PCNA阳性肝细胞数量显著增加。急性乙醇暴露导致肝脏出现退行性形态学变化。与对照组相比,乙醇组血液中谷胱甘肽水平降低,血清碱性磷酸酶和天冬氨酸转氨酶活性增加。与其他组相比,给予乙醇组的肝脏中谷胱甘肽水平降低,但脂质过氧化增加。乙醇组给予硫酸锌后,退行性变化、脂质过氧化以及碱性磷酸酶和天冬氨酸转氨酶活性显著降低,但肝脏谷胱甘肽增加。
硫酸锌对乙醇诱导的肝损伤具有保护作用。此外,细胞增殖可能与给予乙醇+硫酸锌的大鼠肝脏中金属硫蛋白免疫反应性增加有关。