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Melatonin prevents disruption of hepatic reactive oxygen species metabolism in rats treated with carbon tetrachloride.
Journal of Pineal Research ( IF 10.3 ) Pub Date : 2003-12-17 , DOI: 10.1046/j.1600-079x.2003.00091.x
Yoshiji Ohta 1 , Mutsumi Kongo-Nishimura , Tatsuya Matsura , Kazuo Yamada , Akira Kitagawa , Teruaki Kishikawa
Affiliation  

We reported that melatonin prevents the progression of carbon tetrachloride (CCl4)-induced acute liver injury in rats possibly by attenuating enhanced lipid peroxidation and reduced glutathione depletion. Herein, we examined the effect of melatonin on the changes in hepatic reactive oxygen species (ROS) metabolism in rats with a single intraperitoneal injection of CCl4 (1.6 g/kg body weight); the intent was to clarify the therapeutic mechanism of the indoleamine on CCl4-induced acute liver injury. Rats with and without CCl4 treatment received a single oral dose of melatonin (10, 50 or 100 mg/kg body weight) 6 hr after CCl4 treatment. Hepatic concentrations of ascorbic acid (ASC) and vitamin E (VE) and hepatic activities of superoxide dismutase (SOD), catalase (CAT), Se-glutathione peroxidase (Se-GSH-Px), glutathione reductase (GSSG-R), glucose-6-phosphate dehydrogenase (G-6-PDH), and xanthine oxidase (XO) were determined 6 and 24 hr after CCl4 treatment. The liver of CCl4-treated rats showed reductions in ASC concentrations, and SOD activity and an increase in G-6-PDH activity at 6 hr after treatment and further decreases in ACS concentrations and SOD activity and also further increase in G-6-PDH activity in addition to decreases in CAT and GSSG-R activities and increases in VE concentrations and XO activity at 24 hr after treatment. Melatonin attenuated the reductions in hepatic ASC concentrations and SOD, CAT and GSSG-R activities and the increase in hepatic XO activity in a dose-dependent manner without affecting either hepatic Se-GSH-Px activity or the increased hepatic VE concentration and G-6-PDH activity at 24 hr after CCl4 treatment. No dose of melatonin influenced hepatic ACS and VE concentrations and SOD, CAT, Se-GSH-Px, G-6-PDH, and XO activities in CCl4-untreated rats. These results indicate that melatonin postadministered at pharmacological doses prevents the disruption of hepatic ROS metabolism associated with ASC, SOD, CAT, GSSG-R, and XO, in addition to reduced glutathione, in CCl4-treated rats.

中文翻译:

褪黑素可防止四氯化碳处理的大鼠肝中活性氧代谢中断。

我们报告说,褪黑激素可能通过减弱增强的脂质过氧化作用和减少的谷胱甘肽消耗来阻止四氯化碳(CCl4)诱导的大鼠急性肝损伤的进展。在本文中,我们研究了褪黑素对腹腔注射CCl4(1.6 g / kg体重)大鼠肝活性氧(ROS)代谢变化的影响;目的是阐明吲哚胺对CCl4诱导的急性肝损伤的治疗机制。接受和不接受CCl4治疗的大鼠在CCl4治疗后6小时接受了单次口服褪黑激素(10、50或100 mg / kg体重)。肝中抗坏血酸(ASC)和维生素E(VE)的浓度以及超氧化物歧化酶(SOD),过氧化氢酶(CAT),硒谷胱甘肽过氧化物酶(Se-GSH-Px),谷胱甘肽还原酶(GSSG-R)的肝活性,在CCl4处理后6和24小时确定了葡萄糖-6-磷酸脱氢酶(G-6-PDH)和黄嘌呤氧化酶(XO)。经CCl4处理的大鼠的肝脏在治疗后6小时显示出ASC浓度降低,SOD活性降低以及G-6-PDH活性升高,ACS浓度和SOD活性进一步降低,G-6-PDH进一步升高处理后24小时,CAT和GSSG-R活性降低,VE浓度和XO活性增加。褪黑素以剂量依赖的方式减弱了肝脏ASC浓度和SOD,CAT和GSSG-R活性的降低以及肝脏XO活性的增加,而没有影响肝脏Se-GSH-Px活性或增加的肝VE浓度和G-6 CCl4处理后24小时的-PDH活性。没有剂量的褪黑素会影响未经CCl4处理的大鼠的肝ACS和VE浓度以及SOD,CAT,Se-GSH-Px,G-6-PDH和XO活性。这些结果表明,褪黑激素以药理剂量后给药,除了降低谷胱甘肽外,还可以防止与ASC,SOD,CAT,GSSG-R和XO关联的肝ROS代谢的中断,而CCl4处理的大鼠中则没有。
更新日期:2019-11-01
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