Quercetin protects HCT116 cells from Dichlorvos-induced oxidative stress and apoptosis

被引：25

作者：

Ben Salem, Intidhar ^{[1
,2
]}

Boussabbeh, Manel ^{[1
,2
]}

Graiet, Imen ^{[1
]}

Rhouma, Asma ^{[1
]}

Bacha, Hassen ^{[1
]}

Essefi, Salwa Abid ^{[1
]}

机构：

[1] Fac Med Dent, Lab Res Biol Compatible Cpds, Monastir 5000, Tunisia

[2] Carthage Univ, Fac Sci Bizerte, Tunis, Tunisia

来源：

CELL STRESS & CHAPERONES | 2016年 / 21卷 / 01期

关键词：

Dichlorvos; Quercetin; Oxidative stress; Apoptosis; DNA fragmentation; LIPID-PEROXIDATION; GENE-EXPRESSION; NADPH OXIDASE; VITAMIN-E; TOXICITY; ORGANOPHOSPHATE; CHLORPYRIFOS; EXPOSURE; DAMAGE; DEATH;

D O I：

10.1007/s12192-015-0651-7

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The present study was designed to assess the possible protective effects of Quercetin (QUER), a flavonoid with well-known pharmacological effects, against Dichlorvos (DDVP)-induced toxicity in vitro using HCT116 cells. The cytotoxicity was monitored by cell viability, reactive oxygen species (ROS) generation, anti-oxidant enzyme activities, malondialdehyde (MDA) production, and DNA fragmentation. The apoptosis was assessed through the measurement of the mitochondrial transmembrane potential (Delta Im) and caspase activation. The results indicated that pretreatment of HCT116 cells with QUER, 2 h prior to DDVP exposure, significantly decreased the DDVP-induced cell death, inhibited the ROS generation, modulated the activities of catalase (CAT) and superoxide dismutase (SOD), and reduced the MDA level. The reductions in mitochondrial membrane potential, DNA fragmentation, and caspase activation were also attenuated by QUER. These findings suggest that dietary QUER can protect HCT116 cells against DDVP-induced oxidative stress and apoptosis.

引用

页码：179 / 186

页数：8

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