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维生素 E 对展青霉素细胞毒性和遗传毒性的抗氧化和抗原毒作用在 HepG2 细胞中的研究。

Antioxidative and antigenotoxic effect of vitamin E against patulin cytotoxicity and genotoxicity in HepG2 cells.

机构信息

Laboratory for Research on Biologically Compatible Compounds-LRSBC, Monastir University, Rue Avicenne, Monastir 5019, Tunisia.

出版信息

Environ Toxicol. 2013 Jun;28(6):299-306. doi: 10.1002/tox.20720. Epub 2011 Jun 7.

DOI:10.1002/tox.20720
PMID:21656641
Abstract

Patulin (PAT) is a mycotoxin produced in fruits, mainly in apples, by certain species of Penicillium, Aspergillus, and Byssochlamys. It has been shown that PAT is cytotoxic, genotoxic, and mutagenic in different cell types. Several studies incriminate the oxidative stress as a mechanism of PAT-mediated toxicity. In this context, our aim was to investigate the protective role of Vitamin E (Vit E), an antioxidant agent, against PAT induced cytotoxicity and genotoxicity in cultured HepG2 cells. The obtained results showed that addition of Vit E in cells treated with PAT significantly reduce cell mortality induced by this toxin. In the same conditions, Vit E decreased the intracellular level of ROS, reduced PAT induced p53 expression, and reversed PAT induced DNA damage. In addition, Vit E prevented significantly the percentage of chromosome aberrations induced by PAT in HepG2 cells in a concentration dependant manner. These results suggest that Vit E, an exogenous antioxidant agent, plays an important role in defense against PAT-induced cytotoxicity and genotoxicity, which confirms the involvement of oxidative stress in the induction of DNA damage by PAT in HepG2 cells.

摘要

棒曲霉素(PAT)是由某些青霉、曲霉和蝙蝠蛾属真菌在水果中产生的一种真菌毒素,主要存在于苹果中。研究表明,PAT 在不同细胞类型中具有细胞毒性、遗传毒性和致突变性。一些研究将氧化应激作为 PAT 介导的毒性的一种机制。在这种情况下,我们的目的是研究维生素 E(Vit E)作为一种抗氧化剂,对 PAT 诱导的培养 HepG2 细胞毒性和遗传毒性的保护作用。研究结果表明,在加入 PAT 的细胞中添加 Vit E 可显著降低该毒素引起的细胞死亡率。在相同条件下,Vit E 降低了细胞内 ROS 水平,减少了 PAT 诱导的 p53 表达,并逆转了 PAT 诱导的 DNA 损伤。此外,Vit E 以浓度依赖的方式显著防止 PAT 诱导的 HepG2 细胞染色体畸变的百分比。这些结果表明,Vit E 作为一种外源性抗氧化剂,在防御 PAT 诱导的细胞毒性和遗传毒性方面发挥着重要作用,这证实了氧化应激在 PAT 诱导 HepG2 细胞 DNA 损伤中的作用。

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