{"title":"Effect of sodium selenite on lipids and lipid-metabolizing enzymes in N-nitrosodiethylamine-induced hepatoma-bearing rats","authors":"C. Thirunavukkarasu, K. Selvedhiran, J. Prince Vijaya Singh, P. Senthilnathan, D. Sakthisekaran","doi":"10.1002/jtra.10018","DOIUrl":null,"url":null,"abstract":"As part of a substantial effort to curtail the adverse health effects posed by hepatoma, studies have been conducted to elucidate the possible mechanism for the anticarcinogenic action of sodium selenite against N-nitrosodiethylamine-induced hepatoma. Several investigations recognize selenium as potent antioxidant, as well as an anticarcinogen, in both animal and human systems. Sodium selenite was administered to Wistar rats bearing hepatoma induced by N-nitrosodiethylamine to study the alterations in the concentration of lipid profiles and in activities of some lipid-metabolizing enzymes. Control and tumor-bearing animals were fed 4 ppm of sodium selenite before initiation or during initiation and/or during promotion phases of carcinogenesis. Hepatic total cholesterol, free cholesterol, triglycerides, free fatty acids, and phospholipids were significantly lowered, whereas cholesterol esters was greater because of selenite administration in N-nitrosodiethylamine-induced tumor-bearing rats. Total lipase, lipoprotein lipase, lecithin: cholesterol acyl transferase, and cholesterol ester synthetase registered greater activities in hepatoma of selenite administered rats with tumor whereas the activity of cholesterol ester hydrolase in hepatoma-bearing animals was lower as a result of selenite administration. These observations clearly indicate the effect of selenite in correcting the abnormalities of lipid metabolism in tumor-induced animals. Previous evidence from this laboratory and present observations it can be concluded that the anticancer property of selenite my also be by its strong hypolipidemic capacity in vivo system. J. Trace Elem. Exp. Med. 16:1–15, 2003. © 2003 Wiley-Liss, Inc.","PeriodicalId":101243,"journal":{"name":"The Journal of Trace Elements in Experimental Medicine","volume":"16 1","pages":"1-15"},"PeriodicalIF":0.0000,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/jtra.10018","citationCount":"5","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Journal of Trace Elements in Experimental Medicine","FirstCategoryId":"1085","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/jtra.10018","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 5
亚硒酸钠对N-亚硝基二乙胺诱导肝癌大鼠脂质及脂质代谢酶的影响
作为减少肝癌对健康造成的不良影响的实质性努力的一部分,已经进行了研究,以阐明亚硒酸钠对N-亚硝基二乙胺诱导的肝癌的抗癌作用的可能机制。几项研究表明,硒在动物和人类系统中都是一种强效抗氧化剂和抗癌原。用亚硒酸钠对N-亚硝基二乙胺诱发的Wistar大鼠肝癌进行研究,以研究脂质浓度和某些脂质代谢酶活性的变化。对照和荷瘤动物在致癌作用开始前、开始期间和/或促进阶段喂食4ppm的亚硒酸钠。在N-亚硝基二乙胺诱导的荷瘤大鼠中,肝脏总胆固醇、游离胆固醇、甘油三酯、游离脂肪酸和磷脂显著降低,而胆固醇酯更高,因为亚硒酸盐给药。总脂肪酶、脂蛋白脂肪酶、卵磷脂:胆固醇酰基转移酶和胆固醇酯合成酶在亚硒酸盐给药的肿瘤大鼠的肝癌中表现出更高的活性,而携带肝癌的动物的胆固醇酯水解酶的活性由于亚硒酸酯给药而较低。这些观察结果清楚地表明亚硒酸盐在纠正肿瘤诱导的动物脂质代谢异常中的作用。该实验室先前的证据和目前的观察结果可以得出结论,亚硒酸盐的抗癌特性也可能是由于其在体内系统中具有强大的降血脂能力。J.Trace Elem。Exp.Med.16:1–152003。©2003 Wiley-Liss,股份有限公司。
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