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Inhibition of Sudan I genotoxicity in human liver-derived HepG2 cells by the antioxidant hydroxytyrosol

机译:抗氧化剂羟基酪醇抑制苏丹I对人肝源性HepG2细胞的遗传毒性

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摘要

The chemoprotective effect of hydroxytyrosol (HT) against Sudan I-induced genotoxicity was investigated in a human hepatoma cell line, HepG2. The comet assay and micronucleus (MN) assay were used to monitor genotoxicity. Intracellular reactive oxygen species (ROS) formation was measured using a fluorescent probe, 2,7-dichlorofluorescein diacetate (DCFH-DA). The levels of oxidative DNA damage and lipid peroxidation were estimated by immunocytochemistry analysis of 8-hydroxydeoxyguanosine (8-OHdG) and by measuring levels of thiobarbituric acid-reactive substances (TBARS), respectively. Intracellular glutathione (GSH) level was estimated by fluorometric methods. The results showed that HT significantly reduced the genotoxicity caused by Sudan I. Furthermore, HT ameliorated lipid pexidation as demonstrated by a reduction in TBARS formation and attenuated GSH depletion in a concentration-dependent manner. It was also found that HT reduced intracellular ROS formation and 8-OHdG level caused by Sudan I. These results strongly suggest that HT has significant protective ability against Sudan I-induced genotoxicity.
机译:在人类肝癌细胞系HepG2中研究了羟基酪醇(HT)对Sudan I诱导的基因毒性的化学保护作用。彗星试验和微核(MN)试验用于监测遗传毒性。使用荧光探针2,7-二氯荧光素二乙酸酯(DCFH-DA)测量细胞内活性氧(ROS)的形成。分别通过8-羟基脱氧鸟苷(8-OHdG)的免疫细胞化学分析和通过测量硫代巴比妥酸反应性物质(TBARS)的水平来估计氧化性DNA损伤和脂质过氧化的水平。细胞内谷胱甘肽(GSH)水平通过荧光法估算。结果表明,HT显着降低了由苏丹I引起的遗传毒性。此外,如TBARS形成减少和GSH耗竭以浓度依赖的方式减弱所证明,HT改善了脂质过剩。还发现HT减少了苏丹I引起的细胞内ROS形成和8-OHdG水平。这些结果强烈表明HT具有抗苏丹I诱导的基因毒性的显着保护能力。

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