Zinc protects HepG2 cells against the oxidative damage and DNA damage induced by ochratoxin A
作者： Juanjuan Zheng , Yu Zhang , Wentao Xu , YunBo Luo , Junran Hao
DOI: 10.1016/J.TAAP.2013.01.021
关键词: Reactive oxygen species 、 Antioxidant 、 Superoxide dismutase 、 Oxidative stress 、 Biology 、 DNA damage 、 Genotoxicity 、 Biochemistry 、 Molecular biology 、 Catalase 、 Zinc 、 Toxicology 、 Pharmacology
摘要: Oxidative stress and DNA damage are the most studied mechanisms by which ochratoxin A (OTA) induces its toxic effects, include nephrotoxicity, hepatotoxicity, immunotoxicity genotoxicity. Zinc, is an essential trace element, considered a potential antioxidant. The aim of this paper was to investigate whether zinc supplement could inhibit OTA-induced oxidative in HepG2 cells mechanism inhibition. results indicated that exposure OTA decreased intracellular concentration; significantly reduced production reactive oxygen species (ROS) decrease superoxide dismutase (SOD) activity but did not affect mitochondrial membrane (Δψm). Meanwhile, addition chelator N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN) strongly aggravated damage. This study also demonstrated helped maintain integrity through reduction strand breaks, 8-hydroxy-2'-deoxyguanosine (8-OHdG) formation hypomethylation. increased mRNA expression metallothionein1-A (MT1A), metallothionein2-A (MT2A) Cu/Zn (SOD1). Zinc further enhanced MT1A MT2A, it had no effect on SOD1 catalase (CAT). for first time proven reduce cytotoxicity inhibiting damage, regulating zinc-associated genes. Thus, can potentially be used toxicity contaminated feeds.
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