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燃煤型地方性氟中毒与抗氧化酶活性降低和 Cu/Zn-SOD 基因表达下调有关。

Coal-burning endemic fluorosis is associated with reduced activity in antioxidative enzymes and Cu/Zn-SOD gene expression.

机构信息

Department of Prevention Medicine, School of Public Health, Zunyi Medical College, Zunyi, 563003, People's Republic of China.

出版信息

Environ Geochem Health. 2014 Feb;36(1):107-15. doi: 10.1007/s10653-013-9522-2. Epub 2013 Apr 9.

DOI:10.1007/s10653-013-9522-2
PMID:23567976
Abstract

To study the effect of fluorine on the oxidative stress in coal-burning fluorosis, we investigated the environmental characteristics of coal-burning endemic fluorosis combined with fluorine content surveillance in air, water, food, briquette, and clay binder samples from Bijie region, Guizhou Province, southwest of China. The activities of antioxidant enzymes including copper/zinc superoxide dismutase (Cu/Zn-SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and level of lipid peroxidation such as malondialdehyde (MDA) were measured in serum samples obtained from subjects residing in the Bijie region. Expression of the Cu/Zn-SOD gene was assessed by quantitative reverse transcriptase PCR (qRT-PCR). Our results showed that people suffering from endemic fluorosis (the high and low exposure groups) had much higher MDA level. Their antioxidant enzyme activities and Cu/Zn-SOD gene expression levels were lower when compared to healthy people (the control group). Fluorosis can decrease the activities of antioxidant enzymes, which was associated with exposure level of fluorine. Down-regulation of Cu/Zn-SOD expression may play an important role in the aggravation of oxidative stress in endemic fluorosis.

摘要

为了研究氟对燃煤型氟中毒(endemic fluorosis)患者氧化应激的影响,我们结合贵州省毕节地区的空气、水、食物、煤球和黏土黏合剂样本中的氟含量监测,对该地区的环境特征进行了研究。本研究在毕节地区采集了血清样本,检测了血清样本中抗氧化酶(包括铜/锌超氧化物歧化酶(Cu/Zn-SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px))的活性以及丙二醛(MDA)等脂质过氧化产物的水平。采用实时荧光定量聚合酶链式反应(qRT-PCR)评估了 Cu/Zn-SOD 基因的表达情况。结果表明,氟中毒患者(高暴露组和低暴露组)的 MDA 水平明显较高。与健康人(对照组)相比,氟中毒患者的抗氧化酶活性和 Cu/Zn-SOD 基因表达水平较低。氟中毒会降低抗氧化酶的活性,这与氟暴露水平有关。Cu/Zn-SOD 表达下调可能在氟中毒氧化应激的加重中发挥重要作用。

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