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肌肽对甲基乙二醛诱导的大鼠氧化应激的影响。

The effect of carnosine on methylglyoxal-induced oxidative stress in rats.

作者信息

Yılmaz Zülbiye, Kalaz Esra Betül, Aydın A Fatih, Soluk-Tekkeşin Merva, Doğru-Abbasoğlu Semra, Uysal Müjdat, Koçak-Toker Necla

机构信息

a Department of Biochemistry , Istanbul Medical Faculty, Istanbul University , Istanbul , Turkey , and.

b Department of Pathology, Oncology Institute , Istanbul University , Istanbul , Turkey.

出版信息

Arch Physiol Biochem. 2017 Jul;123(3):192-198. doi: 10.1080/13813455.2017.1296468. Epub 2017 Mar 6.

DOI:10.1080/13813455.2017.1296468
PMID:28276708
Abstract

Methylglyoxal (MG) is generated from glycolytic metabolites, lipid peroxidation, glucose autooxidation and protein glycation. It is a prooxidant inducing oxidative stress and formation of advanced glycation end products (AGE). Effect of carnosine (CAR) as an antioxidant on toxicity due to MG has generated interest. In this study, rats were given incrementally increased doses (100-300 mg/kg) of MG in drinking water for ten weeks. CAR (250 mg/kg i.p.) was administered with MG. Plasma thiobarbituric reactive substances (TBARS), protein carbonyl (PC), advanced oxidation protein products (AOPP) and AGE levels were elevated by MG, and CAR decreased PC, AOPP and AGE levels. MG increased liver reactive oxygen species (ROS), TBARS, PC and AOPP levels, which were decreased by CAR. Thus, in vivo role of CAR on chronic MG administration was observed to suppress the generated hepatic and plasma oxidative stress.

摘要

甲基乙二醛(MG)由糖酵解代谢产物、脂质过氧化、葡萄糖自氧化和蛋白质糖基化产生。它是一种促氧化剂,可诱导氧化应激并形成晚期糖基化终产物(AGE)。肌肽(CAR)作为抗氧化剂对MG毒性的影响已引起关注。在本研究中,给大鼠饮用含剂量递增(100 - 300 mg/kg)MG的水,持续十周。同时给大鼠腹腔注射CAR(250 mg/kg)。MG使血浆硫代巴比妥酸反应性物质(TBARS)、蛋白质羰基(PC)、晚期氧化蛋白产物(AOPP)和AGE水平升高,而CAR降低了PC、AOPP和AGE水平。MG增加了肝脏活性氧(ROS)、TBARS、PC和AOPP水平,而CAR使其降低。因此,观察到CAR在慢性给予MG的体内作用是抑制所产生的肝脏和血浆氧化应激。

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