补充α -生育酚对成年小鼠的影响:维生素E调控基因的生化状态、组织病理学分析和综述

H. Poaty, Franck Arnaud Moukobolo Kinsangou, E. Mokondjimobé
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引用次数: 0

摘要

维生素E (VE)是一种抗氧化防御系统和信号分子,已成为癌症化学预防或化疗后辅助治疗的各种临床试验的主题。在某些情况下,它被认为是一种促氧化剂,可诱发癌症转移或糖尿病等不良反应。本研究的目的首先是研究维生素E (α-T)对小鼠的影响,以评估其发生糖尿病的风险;其次是对维生素E调节基因进行综述。这项研究是在32只成年白化小鼠身上进行的,它们以不同的剂量给予α -生育酚。然后分析血液生化指标状况。通过组织病理学分析研究肾损害。通过检索基因数据库、PubMed Central和Google scholar对VE调控基因进行综述。血液生化参数,特别是血糖水平、高脂血症和高肌酐血症的不充分状态已被观察到。肾脏损伤伴结构改变。强调了一系列由VE调节的基因,这些基因可以解释α-T诱导糖尿病的发生机制。研究表明,大剂量α-T的补充可导致大鼠肾脏生化指标紊乱,肾脏组织功能紊乱,并发糖尿病。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of Alpha-Tocopherol Supplementation on Adult Mices: Biochemichal Status, Histopathological Analysis and Review of Genes Modulated by Vitamin E
Vitamin E (VE) is an antioxydant defense system and a signaling molecule which has been the subject of various clinical trials in cancer chemoprevention or in adjuvant therapy after chemotherapy. In some circunstances it is indexed to act as a pro-oxidant inducing adverse effects such as progesssion of cancer metastasis or diabetes. The objective of this work is firstly to investigated the effect of VE (α-T) supplementation on mices, in way to evaluate the risk in developping diabetes and secondly to make review on vitamin E modulated genes. The study was performed on 32 adult albino mices in which alpha-tocopherol was administred at different doses. After, blood biochemical paramaters status has been analysed. Renal damages were researched by histopathological analysis. We have made review on VE modulated genes through indexed articles in genetic databases, PubMed Central and Google scholar. An inadequate status of blood biochemical paramaters especially, glucose level, hyperlipidemia and a hypercreatininemia has been observed. Renal damages with modifications in structures were noted. A list of genes modulated by VE, which could explain mechanisms by which α-T- induced diabetes could appear was highlighted. The study shows that high doses of α-T supplement resulted in disorder of biochemical parameters, with dysfunction of renal tissue and development of diabetes.
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