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基于多胺水平的调节,亚硒酸钠对N-亚硝基二乙胺诱导及苯巴比妥促进的大鼠肝脏肿瘤发生的抑制作用。

The inhibitory effect of sodium selenite on N-nitrosodiethylamine-induced and phenobarbital promoted liver tumourigenesis in rats based on the modulation of polyamine levels.

作者信息

Thirunavukkarasu C, Premkumar K, Jagadeeswaran R, Sakthisekaran D

机构信息

Department of Medical Biochemistry, Dr ALM Post-Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai, 600 113, India.

出版信息

Mol Cell Biochem. 2005 Dec;280(1-2):165-72. doi: 10.1007/s11010-005-8907-7.

Abstract

In the present study, we have evaluated the effects of dietary selenite (Se) on polyamine levels and its influence on N-nitrosodiethylamine (DEN) initiated and Phenobarbital (PB) promoted in rat liver carcinogenesis. Dietary selenite at a concentration of 4 ppm (through drinking water) was administered in rats either before initiation (4 weeks), or during promotion (16 weeks) and entire experimental period (20 weeks). Male Wistar strain of albino rats was treated with single intra peritoneal dose of DEN (200 mg kg(-1) body weight), after 2 weeks the carcinogenic effect was promoted by PB (0.05%; through diet). Alpha fetoprotein (AFP) was investigated after the 20th-week of experimental period. Selenite-treated animals markedly reduced the AFP during the time of pre-selenite [before initiation (4 weeks)] and entire experimental period (20 weeks), administration rather than the promotion period. This infers that anticancer property of selenite depends on the stage of carcinogenesis, rather than duration of treatment. Evaluation of polyamine levels in hepatoma and surrounding liver tissue showed significant difference in the selenite-treated groups compared with pair-fed control groups. Furthermore, histopathological examination showing remarkable difference between control and treated groups. These results demonstrate that selenite can modulate the development of DEN-induced and PB-promoted rat liver carcinogenesis through a polyamine-dependent mechanism.

摘要

在本研究中,我们评估了膳食亚硒酸盐(Se)对多胺水平的影响及其对N-亚硝基二乙胺(DEN)启动和苯巴比妥(PB)促进大鼠肝癌发生的影响。以4 ppm的浓度(通过饮用水)给大鼠喂食亚硒酸盐,给药时间分别为启动前(4周)、促进期(16周)或整个实验期(20周)。对白化雄性Wistar大鼠腹腔注射单剂量DEN(200 mg kg⁻¹体重),2周后用PB(0.05%;通过饮食)促进致癌作用。在实验期第20周后检测甲胎蛋白(AFP)。亚硒酸盐处理的动物在亚硒酸盐给药前(启动前4周)和整个实验期(20周),而非促进期,AFP水平显著降低。这表明亚硒酸盐的抗癌特性取决于致癌作用的阶段,而非治疗持续时间。对肝癌组织和周围肝组织中多胺水平的评估显示,与配对喂养的对照组相比,亚硒酸盐处理组有显著差异。此外,组织病理学检查显示对照组和处理组之间有明显差异。这些结果表明,亚硒酸盐可通过多胺依赖性机制调节DEN诱导和PB促进的大鼠肝癌发生。

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