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茶儿茶素对活性氧诱导的脂质、蛋白质和2-脱氧核糖降解的体外保护作用。

In vitro protection of reactive oxygen species-induced degradation of lipids, proteins and 2-deoxyribose by tea catechins.

作者信息

Raza H, John A

机构信息

Department of Biochemistry, Faculty of Medicine and Health Sciences, P.O. Box 17666, UAE University, Al Ain, United Arab Emirates.

出版信息

Food Chem Toxicol. 2007 Oct;45(10):1814-20. doi: 10.1016/j.fct.2007.03.017. Epub 2007 Mar 31.

DOI:10.1016/j.fct.2007.03.017
PMID:17490800
Abstract

Both the anti- and pro-oxidant effects of tea catechins, have been implicated in the alterations of cellular functions which determine their chemoprotective and therapeutic potentials in toxicity and diseases. Here, we have studied the protective mechanism (s) of three main green tea catechins namely, epicatechin (EC), epicatechin gallate (ECG) and epigallocatechin gallate (EGCG) on free radical induced oxidative degradation of membrane lipids and proteins under in vitro conditions using isolated cell free fractions from rat liver. In addition, we have also studied the effects of the tea catechins on 2-deoxyribose degradation in the presence of Fenton and Haber-Weiss oxidants. Glutathione S-transferase and cytochrome P450 2E1 activities and lipid peroxidation were found to be markedly inhibited by tea catechins. These catechins also inhibited the reactive oxygen species formation and oxidative carbonylation of subcellular proteins induced by a physiological oxidant, 4-hydroxynonenal. EGCG and the other catechins showed a time and concentration-dependent effects on the degradation of 2-deoxyribose in the presence of Fenton oxidants. Our results indicate that tea catechins prevent molecular degradation in oxidative stress conditions by directly altering the subcellular ROS production, glutathione metabolism and cytochrome P450 2E1 activity. These results may have implications in determining the chemotherapeutic use of tea catechins in oxidative stress related diseases.

摘要

茶儿茶素的抗氧化和促氧化作用均与细胞功能的改变有关,这些改变决定了它们在毒性和疾病中的化学保护和治疗潜力。在此,我们使用大鼠肝脏分离的无细胞组分,在体外条件下研究了三种主要绿茶儿茶素,即表儿茶素(EC)、表儿茶素没食子酸酯(ECG)和表没食子儿茶素没食子酸酯(EGCG)对自由基诱导的膜脂质和蛋白质氧化降解的保护机制。此外,我们还研究了茶儿茶素在芬顿和哈伯-维伊斯氧化剂存在下对2-脱氧核糖降解的影响。发现谷胱甘肽S-转移酶和细胞色素P450 2E1活性以及脂质过氧化受到茶儿茶素的显著抑制。这些儿茶素还抑制了由生理氧化剂4-羟基壬烯醛诱导的亚细胞蛋白质的活性氧形成和氧化羰基化。在芬顿氧化剂存在下,EGCG和其他儿茶素对2-脱氧核糖的降解表现出时间和浓度依赖性影响。我们的结果表明,茶儿茶素通过直接改变亚细胞活性氧的产生、谷胱甘肽代谢和细胞色素P450 2E1活性,在氧化应激条件下预防分子降解。这些结果可能对确定茶儿茶素在氧化应激相关疾病中的化疗用途具有启示意义。

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