谷胱甘肽- s -转移酶(GSTM1和GSTT1)多态性与铅环境暴露个体的铅毒性

S Rabiu, MG Abubakar, DM Sahabi, MA Makusidi, SAMAS Eqani
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摘要

参与金属解毒的酶的遗传变异可能影响铅诱导的氧化应激的易感性。本研究旨在评价谷胱甘肽- s -转移酶基因遗传变异对铅环境暴露个体氧化应激标志物(GSH、SOD、CAT和MDA)的影响。聚合酶链反应检测GSTM1和GSTT1的零纯合基因型。采用微波等离子体原子发射光谱(MP- AES-Agilent 4210 USA)测定血铅水平。超氧化物歧化酶、过氧化氢酶和谷胱甘肽活性采用开曼商用试剂盒检测。研究发现,研究对象的平均血铅水平为78.16±5.79微克/分升,范围为26.6至191.0微克/分升。GSTM1和GSTT1无效基因型的频率分别为23%和50.8%。在血铅水平大于70微克/分升的个体中,这种频率很高。GSTM1和GSTT1基因型个体抗氧化酶(SOD)和CAT活性显著降低,谷胱甘肽水平显著降低,MDA浓度显著升高。因此,这项研究的结果足以推断环境暴露于铅和氧化应激之间的因果关系。GSTM1和GSTT1位点同源null的个体易因环境暴露于铅而增加多器官毒性风险。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Glutathione-S-transferase (GSTM1 and GSTT1) polymorphism and lead toxicity in individuals environmentally exposed to lead
Genetic variation in enzymes involved in metal detoxification could have influence on susceptibility to lead-induced oxidative stress. The present study aimed at evaluating the effects of genetic variation of Glutathione-S- transferase gene on oxidative stress markers (GSH, SOD, CAT and MDA) among individuals environmentally exposed to lead. GSTM1 and GSTT1 null homozygous genotypes were determined by polymerase chain reaction. Blood lead levels were determined using Microwave Plasma Atomic Emission Spectroscopy (MP- AES-Agilent 4210 USA). Activities of superoxide dismutase, catalase and glutathione levels were assayed using Cayman’s commercial kits. The study found mean blood lead levels of the study subjects of 78.16± 5.79µg/dl with range from 26.6 to 191.0 µg/dl. The frequencies of GSTM1 and GSTT1 null genotypes were 23% and 50.8% respectively. The frequency was high in individuals with blood lead levels greater than 70µg/dl. Significant decreased activity of antioxidant enzymes (SOD and CAT), glutathione levels and concomitant increased of MDA concentrations were observed in individuals with GSTM1 and GSTT1 null genotypes. Therefore, findings from this study were enough to infer a causal relationship between environmental exposure to lead and oxidative stress. Individuals who are homologous null at GSTM1 and GSTT1 loci predispose to increased risk of multi-organs toxicity from environmental exposure to lead.
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