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二烯丙基二硫对 N-亚硝二乙胺诱导大鼠肝癌形成过程中环流脂质过氧化产物和抗氧化剂时相模式的影响。

Influence of diallyl disulphide on temporal patterns of circulatory lipid peroxidation products and antioxidants in N-nitrosodiethylamine-induced hepatocarcinogenesis in rats.

机构信息

Department of Biochemistry, Faculty of Science, Annamalai University, Annamalainagar, 608 002, Tamil Nadu, India.

出版信息

Toxicol Mech Methods. 2007;17(1):25-32. doi: 10.1080/15376510600885042.

Abstract

ABSTRACT Investigations on the effects of diallyl disulphide (60 mg/kg body weight) orally administered (thrice a week) on the temporal patterns of thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), catalase, and reduced glutathione (GSH) during N-Nitrosodiethylamine (NDEA)-induced hepatocarcinogenesis were performed in rats. The acrophase of TBARS was found to be delayed and of antioxidants was found to be advanced in NDEA-treated rats. The increase in mesor of TBARS, decrease in mesor of antioxidants, and altered amplitude and acrophase indicated the negative imbalance of oxidant and antioxidant occurring during carcinogenesis. Oral treatment of diallyl disulphide (DADS) results in the resynchronization of the altered rhythms of TBARS and other antioxidants. Although NDEA has no known significant effects on the suprachaismatic nucleus (SCN), from the present results it could be hypothesized that it would influence the peripheral oscillator systems, such as liver, possibly by modulating secretion of the various hormones and growth factors during hepatocarcinogenesis.

摘要

摘要 本研究旨在探讨二烯丙基二硫(60mg/kg 体重)经口(每周三次)给药对 N-亚硝二乙胺(NDEA)诱导的肝癌发生过程中硫代巴比妥酸反应物质(TBARS)、超氧化物歧化酶(SOD)、过氧化氢酶和还原型谷胱甘肽(GSH)时间模式的影响。结果发现,NDEA 处理组的 TBARS 峰相位延迟,而抗氧化剂的峰相位提前。TBARS 的中值增加、抗氧化剂的中值减少以及幅度和峰相位的改变表明,在癌变过程中发生了氧化应激和抗氧化失衡。二烯丙基二硫(DADS)的口服治疗导致 TBARS 和其他抗氧化剂的改变节律重新同步。尽管 NDEA 对视交叉上核(SCN)没有明显的已知影响,但从目前的结果可以假设,它可能会通过调节肝癌发生过程中各种激素和生长因子的分泌,影响外周振荡器系统,如肝脏。

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