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首页> 外文期刊>Cell biology international. >1alpha, 25-Dihydroxyvitamin D3 suppresses the effect of streptozotocin-induced diabetes during chemical rat liver carcinogenesis.
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1alpha, 25-Dihydroxyvitamin D3 suppresses the effect of streptozotocin-induced diabetes during chemical rat liver carcinogenesis.

机译：1alpha，25-Dihydroxyvitamin D3在化学大鼠肝癌发生过程中抑制链脲佐菌素诱导的糖尿病的作用。

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The effect of streptozotocin-induced diabetes in male Sprague-Dawley rats was investigated to ascertain whether it has had any modulating role in hepatocarcinogenesis. Hepatocarcinogenesis was initiated with a single sub-necrogenic dose of diethylnitrosamine (DEN) (125 mg/kg body weight, i.p.) whilst acute diabetes was produced with a single i.p. injection of streptozotocin (STZ) (65 mg/kg body weight). STZ was administered either before or after initiation with DEN at 3-week intervals. With this basic experimental regimen, the effect of an antioxidant vitamin, 1alpha, 25-dihydroxyvitamin D3 (VD) (0.3 microg/ 0.1 ml propylene glycol per os twice a week), was investigated with effect from 4 weeks prior to the exposure of DEN or STZ. Primary routine histopathology, hepatic nodular morphometric analysis and major preneoplastic antioxidant and drug metabolising enzymes were tested either with or without VD treatment in different experimental and control groups. Observation of the hepatic nodulogenesis, pathology and level of the antioxidant and drug metabolising enzyme pattern of the tissue showed a marked protection in different experimental groups of rats treated with VD. It may be that VD could elicit an anticarcinogenic potential in the aforesaid regimen by resetting the effects of these biomarkers induced by DEN and/or STZ. We further propose that STZ, when administered 3 weeks after DEN, caused massive damage where its action in vivo could be comparable with any known promoter that could propel the process of carcinogenesis more efficiently than when it was applied before the carcinogen. Copyright 2001 Academic Press.
机译：对链脲佐菌素诱发的糖尿病在雄性Sprague-Dawley大鼠中的作用进行了研究，以确定它在肝癌发生中是否具有任何调节作用。肝癌的发生是通过单次致死剂量的二乙基亚硝胺（DEN）（125 mg / kg体重，腹腔注射）开始的，而急性糖尿病是通过一次腹膜内注射产生的。注射链脲佐菌素（STZ）（65 mg / kg体重）。在开始使用DEN之前或之后，以3周的间隔给予STZ。通过这种基本的实验方案，研究了抗氧化剂维生素1α，25-二羟基维生素D3（VD）（每周两次，每次两次，每次0.3微克/ 0.1毫升丙二醇）的作用，从DEN暴露前4周开始或STZ。在不同的实验组和对照组中，无论是否接受VD治疗，均对主要的常规组织病理学，肝结节形态分析以及主要的肿瘤前抗氧化剂和药物代谢酶进行了测试。观察肝结节的发生，病理学和组织中抗氧化剂和药物代谢酶模式的水平，表明在用VD处理的不同实验组的大鼠中都有明显的保护作用。 VD可能通过重置由DEN和/或STZ诱导的这些生物标记物的作用，在上述方案中引发抗癌作用。我们进一步提出，在DEN后3周给药时，STZ会造成严重损害，其体内作用可与任何已知的启动子相媲美，与在致癌物之前应用相比，该启动子可更有效地推动致癌过程。版权所有2001，学术出版社。

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