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作 者:张红艳[1] 吴绪伟[1] 肖谊[1] 陈梅[1] 李志东[1] 李艳丽[1] 唐开发[2]
机构地区:[1]昆明医科大学附属延安医院呼吸一科,昆明650051 [2]贵阳医学院医学科学研究所,贵阳550004
出 处:《中国医科大学学报》2014年第5期432-436,共5页Journal of China Medical University
基 金:云南省应用基础研究基金(2010ZC198)
摘 要:目的探讨谷胱甘肽S-转移酶M1、T1(GSTM1、T1)基因多态性及氧化应激损伤对非小细胞肺癌易感性。方法本病例对照研究包括110名非小细胞肺癌患者(病例组)和100名正常健康对照者(对照组)。所有研究对象外周血基因组DNAGSTM1、T1基因型采用聚合酶链反应(PCR)技术进行检测;外周血清丙二醛(MDA)、一氧化氮(NO)浓度及总抗氧化能力(T-AOC)采用分光光度计检测方法测定。结果 GSTM1、T1基因缺失型及GSTM1/T1缺失型在病例组明显高于对照组(OR1=2.071,P1=0.009;OR2=1.900,P2=0.024;OR3=3.258,P3=0.003)。MDA及NO水平在病例组显著高于对照组(P<0.001),而T-AOC水平则在病例组明显低于对照组(P<0.001)。同时,病例组中GSTM1、T1基因缺失型及GSTM1/T1缺失型亚组MDA及NO浓度水平明显高于野生型亚组,而T-AOC水平明显低于野生型亚组(P均<0.001)。结论氧化损伤在非小细胞肺癌的发生发展过程中可能扮演着重要角色,而GSTM1、T1基因缺失型非小细胞肺癌患者更易受到氧化应激损伤。Objective To investigate the genetic polymorphisms of the glutathione S-transferase M1 and T1 genes(GSTM1 and GSTT1),and evaluate the oxidative damage in patients with non-small lung cancer(N-SCLC). Methods A total of 110 patients with N-SCLC and 100healthy individuals were recruited in this case-control study. Multiplex polymerase chain reaction(PCR)analysis was used to identify the genotypes. The activity of malondialdehyde(MDA),nitric oxide(NO),and the total antioxidant capacity(T-AOC)were detected by spectroscopic analysis using assay kits. Results The frequencies of the GSTM1,T1,and GSTM1/T1 null genotypes in the patient group were significantly higher than those in control group(OR1 =2.071,P1 =0.009;OR2 =1.900,P2 =0.024;OR3 =3.258,P3 =0.003). The activity of MDA and NO were obviously higher in the patient group compared with the control group(P〈0.001),and T-AOC was obviously lower in patient group than those in control group(P〈0.001). The activity of MDA,and NO were higher but the T-AOC were lower in patients with GSTM1,T1 and GSTM1/T1 null genotypes than those in patients with GSTM1,T1 and GSTM1/T1 present genotypes(P〈0.001). Conclusion Our results suggest that oxidative damage may play a important role in patients with N-SCLC,and the N-SCLC patients with GSTM1 and GSTT1 deletion genotypes are more susceptible to oxidative damage.
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