Increased oxidative damage of sperm and seminal plasma in men with idiopathic infertility is higher in patients with glutathione S-transferase Mu-1 null genotype

Aim： To examine whether a relationship exists between glutathione S-transferase Mu-1 （GSTM1） gene polymorphism and the susceptibility of sperm and seminal plasma from patients with idiopathic infertility to oxidative stress. Methods： Fifty-two men with idiopathic infertility and 60 healthy fertile men were recruited to this study. GSTM1 gene polymorphism was determined by polymerase chain reaction （PCR） and both the infertile and control individuals were divided into GSTM1 null and GSTM1 positive groups according to their GSTM1 gene structure. We compared reactive oxygen species （ROS） generation, malondialdehyde （MDA）, protein carbonyls and glutathione （GSH） concentrations, and glutathione S-transferase （GST） activity in seminal plasma and spermatozoa from infertile patients and controls with respect to GSTM1 genotype. Results： Significantly higher levels of oxidative stress and damage markers were found in idiopathic infertile men with the GSTM1 null genotype compared with those with the GSTM1 positive genotype. There was no significant difference in genotype distribution for theGSTM1 variant between the idiopathic infertile subjects and fertile subjects. Patients with the GSTM1 null genotype also had lower sperm concentrations than those with GSTM1 positive genotype. Conclusion： Our results suggest that the susceptibility of sperm and seminal plasma to oxidative stress is significantly greater in idiopathic infertile men with the GSTM1 null genotype compared with those possessing the gene. Therefore, in patients with idiopathic infertility, GSTM1 polymorphism might be an important source of variation in susceptibility of spermatozoa to oxidative damage.

Genetic polymorphism of glutathione S-transferase T1 gene and susceptibility to idiopathic azoospermia or oligospermia in northwestern China

Aim： To investigate the association of glutathione S-transferase T1 （GSTT1） gene polymorphism in patients with idiopathic azoospermia or oligospermia in the northwestern China population. Methods： In the case-control study, GSTT1 genotypes were identified by multiplex polymerase chain reaction （PCR） with peripheral blood DNA samples from 78 patients with idiopathic azoospermia, 103 patients with idiopathic oligospermia and 156 age-matched controls with normal sperm concentration and motility, according to the criteria adapted from World Health Organization guidelines. All of the patients and controls were from northwestern China. Results： There is a significant association between GSTT1 null genotype with idiopathic azoospermia risk （odds ratio [OR]： 2.36, 95% confidence interval [CI]： 1.33-4.20, P = 0.003） or idiopathic oligospermia risk （OR： 2.00, 95% CI： 1.17-3.27, P = 0.010）. Conclusion： GSTT1 null genotype is a predisposing risk factor for sporadic idiopathic azoospermia or oligospermia in northwestern China. （Asian J Androl 2008 Mar; 10： 266-270）

Association of glutathione S-transferase T1 and M1 gene polymorphisms with ischemic stroke risk in the Chinese Han population

Atherosclerosis plays an important role in ischemic stroke, and oxidative stress participates in the entire process of atherosclerosis. Glutathione S-transferase （GST） acting with other antioxidant enzymes can eliminate reactive oxygen species and protect cells against oxidative damage. To assess the association of glutathione S-transferase （GSTT1 and GSTM1） gene polymorphisms with ischemic stroke in the Chinese Han population, the present study selected 315 patients with ischemic stroke and 210 healthy controls for comparison. GSTT1 and GSTM1 genotypes were determined using polymerase chain reactions, electrophoresis and imaging analysis. No obvious evidence of GSTTI-nulI, GSTMI-null and GSTTI/GSTMI-double null genotype distribution differences was found between case and control groups or between genders. Subgroup analysis showed that the risk of stroke was increased when hypertension was accompanied by GSTTl-null （odds ratio （OR） = 2.996, P 〈 0.001） and GSTMl-null （OR = 3.680, P 〈 0.001 ） genotypes; diabetes mellitus was accompanied by GSTTI-null （OR = 1.860, P = 0.031） and GSTMI-null （OR = 2.444, P = 0.002） genotypes, and smokers showed a GSTTl-null genotype （OR = 2.276, P = 0.003）. GSTT1- and GSTMl-null genotypes may interact synergistically with hypertension, diabetes mellitus and smoking to increase the incidence risk of ischemic stroke.

A systemic review of glutathione S-transferase P1 Ile105Val polymorphism and colorectal cancer risk

Objectives： To investigate the correlation between glutathione S-transferase P1 （GSTP1） Ilel05Val polymorphism and colorectal cancer （CRC） risk. Methods： Studies were identified to investigate the association between GSTP1 Ilel05Val polymorphism and CRC risk. Systematic computerized searches of the PubMed, Chinese National Knowledge Infrastructure, WANFANG and SinoMed were performed. Summary odds ratios （OR） and 95% confidence intervals （95 % CI） were used to measure GSTP 1 Ile 105Val polymorphisms and CRC risk. Results： A total of 23 retrospective studies were included in the meta-analysis. During all studies including 6,981 cases and 8,977 controls, sample sizes ranged from 146 to 2,144. Overall, the pooled results revealed that lie 105Val polymorphism was not associated with CRC risk and confused results were found in subgroup analyses. Further meta-analyses were conducted after excluding low-quality studies. GSTP1 Ilel05Val is associated with increased risk of CRC limited in studies with matched control. There was no significant heterogeneity in all genetic comparisons, but heterogeneity existed in subgroup analyses of heterozygous and dominant comparisons. The meta-regression analyses indicated that matched controls were the significant factor influencing between-study heterogeneity in all possible influential factors including published year, ethnicity, source of control, sample size, Hardy-Weinberg equilibrium （HWE） in control and matched controls. Sensitivity analysis revealed the pooled ORs were not changed before and after removal of each single study in all genetic comparisons, indicating the robustness of the results. Conclusions： GSTP1 Ilel05Val might be associated with increased risk of CRC. However, more high- quality case-control studies should be performed to confirm the authenticity of our conclusion.

Rethinking de novo immune hepatitis,an old concept for liver allograft rejection:relevance of glutathione S-transferase T1 mismatch

Antibody-mediated rejection(AMR) in liver transplantation has long been underestimated. The concept of the liver as an organ susceptible to AMR has emerged in recent years, not only in the context of the major histocompatibility complex with the presence of HLA donor-specific antibodies, but also with antigens regarded as "minor", whose role in AMR has been demonstrated. Among them, antibodies against glutathione S-transferase T1 have been found in 100% of patients with de novo autoimmune hepatitis(dn AIH) when studied. In its latest update, the Banff Working Group for liver allograft pathology proposed replacing the term dn AIH with plasma cell(PC)-rich rejection. Antibodies to glutathione S-transferase T1(GSTT1) in null recipients of GSTT1 positive donors have been included as a contributory but nonessential feature of the diagnosis of PC-rich rejection. Also in this update, non-organ-specific anti-nuclear or smooth muscle autoantibodies are no longer included as diagnostic criteria. Although initially found in a proportion of patients with PC-rich rejection, the presence of autoantibodies is misleading since they are not diseasespecific and appear in many different contexts as bystanders. The cellular types and proportions of the inflammatory infiltrates in diagnostic biopsies have been studied in detail very recently. PC-rich rejection biopsies present a characteristic cellular profile with a predominance of T lymphocytes and a high proportion of PCs, close to 30%, of which 16.48% are Ig G4+. New data on the relevance of GSTT1-specific T lymphocytes to PC-rich rejection will be discussed in this review.

T-cell allorecognition of donor glutathione S-transferase T1 in plasma cell-rich rejection

AIM To investigate the role of glutathione S-transferase T1 donor-specific T lymphocytes in plasma cell-rich rejection of liver allografts.METHODS The study group included 22 liver transplant patients. Among them, 18 patients were mismatched for the glutathione S-transferase T1(GSTT1) alleles(don+/rec-), and 4 were matched(don+/rec+). Seven of the mismatched patients produced anti-GSTT1 antibodies and developed plasma cell-rich rejection(former de novo immune hepatitis). For the detection of specific Tlymphocytes, peripheral blood mononuclear cells were collected and stored in liquid nitrogen. The memory T cell response was studied by adding to the cell cultures to a mix of 39 custom-made, 15-mer overlapping peptides, which covered the entire GSTT1 amino acid sequence. The specific cellular response to peptides was analyzed by flow cytometry using the markers CD8, CD4, IL-4 and IFNγ.RESULTS Activation of CD8^+ T cells with different peptides was observed exclusively in the group of patients with plasma-cell rich rejection(3 out of 7), with production of IL-4 and/or IFNγ at a rate of 1%-4.92% depending on the peptides. The CD4^+ response was most common and not exclusive for patients with the disease, where 5 out of 7 showed percentages of activated cells from 1.24% to 31.34%. Additionally, two patients without the disease but with the mismatch had cells that became stimulated with some peptides(1.45%-5.18%). Highly unexpected was the finding of a double positive CD4^+CD8^(low) T cell population that showed the highest degree of activation with some of the peptides in 7 patients with the mismatch, in 4 patients with plasma cell-rich rejection and in 3 patients without the disease. Unfortunately, CD4^+CD8^(low) cells represent 1% of the total number of lymphocytes, and stimulation could not be analyzed in 9 patients due to the low number of gated cells. Cells from the 4 patients included as controls did not show activation with any of the peptides. CONCLUSION Patients with GSTT1 mismatch can develop a specific T-cell response, but the potential role of this response in the pathogenesis of plasma cell-rich rejection is unknown.

Association among Serum Organochlorine Pesticide Residues, Glutathione S-Transferase M1 Genetic Polymorphism and Female Breast Cancer

Background: The purpose of this study was to evaluate the association among serum organochlorine pesticide residues, glutathione S-transferase M1 genetic polymorphism and female breast cancer. Methods: A 1:1 matched case-control study of 140 newly diagnosed breast cancer patients and 140 non-cancer female patients who consulted the five largest hospitals in the Tangshan city from September 2006 to October 2007. Results: The result showed higher risk of breast cancer among subjects with higher levels of serum DDT and HCH residue, the OR was 3.18 (95%CI, 1.11 - 9.07) and 5.02 (95%CI, 1.64 - 16.56).The value of ORe associated with single environmental factor DDT high residues, and ORg associated with single GSTM1 deletion genotype were respectively 3.86 (1.20 - 12.47) and 1.34 (0.36 - 5.08). The OReg associated with combined action of two factors was 5.59 (1.63 - 18.90), and the value of interaction parameters (γ) equaled 1.24. The value of ORe associated with single environmental factor HCH higher residue and ORg associated with single GSTM1 deletion genotype were respectively 2.73 (0.84 - 8.87) and 1.48 (0.49 - 4.60). The value of OReg associated with combined action of two factors was 3.87 (1.18 - 12.68), and γ equaled 1.38. Conclusion: The results indicated that breast cancer occurrence was the combined result of environmental and genetic factors. The concurrent action of GSTM1 deletion genotype and DDT/HCH enhanced the risk of breast cancer.

Genetic dissection of glutathione S-transferase omega-1:identification of novel downstream targets and Alzheimer's disease pathways

Alzheimer's disease(AD)is affected by genetic factors.Polymorphisms in the glutathione S-transfe rase omega-1(Gsto1)gene have been shown by genetic correlation analyses performed in different ethnic populations to be genetic risk factors for AD.Gene expression profile data from BXD recombinant inbred mice were used in combination with genetic and bioinformatic analyses to chara cterize the mechanisms underlying regulation of Gstol variation regulation and to identify network membe rs that may contribute to AD risk or progression.Allele-specific assays confirmed that variation in Gstol expression is controlled by cis-expression quantitative trait loci.We found that Gstol mRNA levels were related to several central nervous system traits,such as glial acidic fibrillary protein levels in the caudate putamen,co rtical gray matter volume,and hippocampus mossy fiber pathway volume.We identified 2168 genes whose expression was highly correlated with that of Gsto1.Some genes were enriched for the most common neurodegenerative diseases.Some Gsto1-related genes identified in this study had previously been identified as susceptibility genes for AD,such as APP,Grin2 b,Ide,and Psenen.To evaluate the relationships between Gstol and candidate network members,we transfected astrocytes with Gstol siRNA and assessed the effect on putative downstream effecto rs.We confirmed that knockdown of Gstol had a significant influence on Pa2g4 expression,suggesting that Pa2g4 may be a downstream effector of Gstol,and that both genes intera ct with other genes in a network during AD pathogenesis.

Frequency of Null Phenotypes of Glutathione S-Transferase M1 and T1 among the Populations of Tabuk (Northwestern Part of Saudi Arabia)

Background: The variability in the distribution of the null phenotypes of GSTM1 and GSTT1, due to total or partial gene deletion resulting in the lack of the active enzyme, has been reported in different populations, especially in ethnically well-defined groups but not in Tabuk. This study investigated the variability in the distribution of the null phenotypes of GSTM1 and GSTT1 in the population of Tabuk (northwestern part of Saudi Arabia). Method: This study was conducted on 200 subjects of Tabuk—northwestern part of Saudi Arabia among which 100 were chronic smokers and 100 were nonsmokers. The subjects were reporting to hospital for routine checkup. All were without past history of any chronic disease and no significant abnormality. GST genotyping was done by multiplex PCR-based methods. The smoker and control groups were compared using a chi-square test with P GSTM1 deletion homozygosity of 14% and 1% was reported among non smokers and smokers, respectively whereas GSTT1 deletion homozygosity of 28% and 6% was reported among non smokers and smokers, respectively. Our results indicate that there are major differences in allelic distribution of GSTM1 and GSTT1 genes between the two groups investigated. Combined analysis of both genes revealed that 15% of smokers and non smokers harbor the deleted genotype of GSTM1 and 34% of smokers and non smokers harbor the deleted genotype of GSTT1 with significant differences. Conclusion: This study enables selecting subgroups among the general population who are more susceptible to DNA damage and will help genetic studies on the association of GST polymorphisms with disease risks and drug effects in Arab population. Studies with a larger sample size are needed to evaluate and confirm the validity of our results.

STUDY OF THE DELETION MUTATION OF GLUTATHIONE S TRANSFERASE M1 GENE AND ITS ROLE IN SUSCEPTIBILITYTO HEPATOCELLULAR CARCINOMA

Objection: To investigate the glutathione S transferase M1 (GSTM1) gene inherent deletion and its relation to prevalence of hepatocellular carcinoma (HCC) in Guangxi, China. Methods: The GSTM1 gene polymorphism of 120 HCC patients and 100 healthy subjects both from the same high aflatoxin B1 (AFB1) contaminated area were detected using PCR technique with special primers. Another 40 patients from AFB1 low risk area were also tested. Results: In HCC high risk area, it was found that the frequencies of GSTM1 null genotype in HCC patients and healthy subjects were 59% and 51% respectively, with no significant difference. However, the frequency of GSTM1-null genotype in control group from AFB1 low risk area was lower than those from high risk area (P<0.01). Conclusion: Populations in this HCC endemic region show a higher rate of GSTM1-null genotype, which may be partially responsible for the susceptibility to AFB1 induced HCC. But the detoxification effect of GSTM1 alone is not sufficient to resist the genetic toxicity of AFB1, especially in those people who expose to excess AFB1. The GSTM1 gene deletion would not be suitable as an independent predictor of susceptibility to HCC.

GSTM1、GSTT1基因缺失与肺癌易感性的关系

目的探讨谷胱苷肽S转移酶M1（GSTM1）、谷胱苷肽S转移酶T1（GSTT1）基因缺失与肺癌发病之间的关系及其与P16表达降低的相关性在肺癌发生中的作用。方法采用PCR技术检测77例肺癌患者和107例健康对照人群中GSTM1、GSTT1基因缺失的频率，以十二烷基磺酸钠（SDS）-聚丙烯酰胺凝胶电泳及蛋白印迹（WeStern—blot）技术测定P16蛋白在正常组织中的表达。结果病例组GSTM1基因缺失频率为58．4％，显著高于对照组缺失频率为42．1％（X^2=4．811，P=0．028），危险度分析OR=1．938，95％CI=1．070～3．509；病例组GSTT1基因缺失频率为57．1％，接近对照组50．5％缺失频率的水平（X^2=0．802，P=0．371）。联合分析表明，2种基因在肺癌发生中具有协同作用。GSTM1空白基因型与GSTM1非空白基因型个体相比、GSTM1／GSTT1联合空白基因型与其他联合多态基因型相比P16表达水平降低，差异有统计学意义（P〈0．05）。结论GSTM1基因缺失或GSTM1、GSTT1基因联合缺失在肺癌患者中发生频率增高，可增加个体患肺癌的易感性；GSTM1基因缺失及GSTM1／GSTT1联合缺失可能与抑癌基因p16的蛋白表达减低有关。

Association between Polymorphisms of Glutathione S-Transferase and Progression to Cervical Cancer in Women from Burkina Faso and Mali

Although persistence of high-risk human papillomavirus infection is the main risk factor, Glutathione S-Transferase highly polymorphic enzyme involved in the metabolism of xenobiotics, is a good candidate gene. The objective of this study was to compare the polymorphisms of Glutathione S-Transferase M1-null in women with cancerous lesions and without lesions. This study consisted of 322 uterine cervix samples of women from Mali and Burkina Faso with Cervical Intra-epithelial Neoplasia 2 and 3, adenocarcinoma and squamous cell carcinoma and 100 women with no lesions. Human Papillomavirus genotyping was performed by Real-time multiplex Polymerase Chain Reaction. Glutathione S-Transferase gene polymorphisms were determined using conventional Polymerase Chain Reaction followed by migration on agarose gel. A statistically significant association with high relative risks of 10.77 for the development of High grade Superficial or Squamous Intra-epithelial Lesion (95% CI = 5.59 - 20.72;p < 0.001), and 13.20 for cancer development (95% CI = 6.79 - 25.63;p < 0.001) was found in women with the null genotype of Glutathione S-Transferase M1 in the study population. In Burkina Faso and Mali, Glutathione S-Transferase M1-null presented relative risks of 9 and 11.05 for high-grade lesions, 15 and 11.40 for cancer. Similarly, significant results had been observed in women with human papillomavirus positive and human papillomavirus negative. The results of the present study support the idea that the deletion of Glutathione S-Transferase M1 plays a crucial role in the progression of high-grade lesions and cervical cancer.

P16基因甲基化和GSTM1基因多态性与非小细胞肺癌易感性研究

[目的]研究P16基因甲基化、谷胱甘肽硫转移酶M1基因(GSTM1)多态性和环境暴露与非小细胞肺癌(NSCLC)的关系。[方法]采用病例对照研究方法选择47例NSCLC患者和94例对照,用甲基化特异性PCR(MSP)检测P16基因甲基化,GSTM1基因多态性用限制性片断长度多态性PCR(PCR-RFLP)测定。[结果]肺癌组接触粉尘、毒物频率高于对照组(P﹤0.01),食用蔬菜水果、饮用消毒水频率肺癌组低于对照组(P﹤0.01);肺癌组织甲基化率44.7%,高于癌旁组织的17%(P﹤0.01),甲基化和吸烟高度相关(P﹤0.01);GSTM1多态性分布无统计学意义(P﹥0.05),粉尘接触、吸烟和GSTM1缺陷型有协同作用,P16甲基化和GSTM1多态性关系不明显。[结论]接触粉尘、毒物明显增加NSCLC危险性,食用蔬菜水果和消毒水降低NSCLC危险性;吸烟致P16基因甲基化参与NSCLC的形成,粉尘、吸烟可能增加GSTM1缺失型患NSCLC危险性,未发现P16甲基化和GSTM1多态性有交互作用。

GSTM1基因多态性与川北地区肺癌易感性关系的研究

目的探讨谷胱苷肽硫转移酶M1（GSTM1）基因多态性与川北地区汉族人群肺癌易感性的关系。方法采用病例对照研究和聚合酶链式反应（PCR）技术检测川北地区125例肺癌患者（肺癌组）和125例非肿瘤患者（对照组）GSTM1基因缺失型的频率,评价其与肺癌易感性的关系。结果 GSTM1缺失基因型[GSTM1（-）]频率在肺癌组和对照组分别为58.4%和56.8%,差异无统计学意义（P=0.822）;GSTM1（-）基因型与肺鳞癌（OR=0.97,95%CI：0.52~1.83,P=0.934）和腺癌（OR=0.94,95%CI：0.42~2.04,P=0.844）风险亦无明确关系。结论 GSTM1各基因型与肺癌风险无明确关系。

肺癌患者及一级亲属GSTM1基因型分析

目的通过检测肺癌患者及其一级亲属谷胱甘肽转硫酶M1(GSTM1)基因型,探讨GSTM1基因作为肺癌遗传易感性标志物的意义。方法采用基于家庭和医院病例的病例对照研究方法,应用双重PCR方法检测其GSTM1基因型。结果肺癌组GSTM1基因缺失率为71.43%(45/63),肺癌亲属组为74.19%(46/62),住院对照组为53.33%(16/30),健康体检组为51.06%(24/47)。肺癌组、肺癌亲属组GSTM1基因缺失率均显著高于健康对照组(P=0.03和0.01);与健康体检组相比肺癌组的OR为2.4(95%CI=1.09～5.29):肺癌亲属组的OR为2.76(95%CI=1.23～6.180)。肺癌亲属组的GSTM1基因缺失率也显著高于住院对照组(P<0.05),OR为2.51(95%CI=1.01～6.24)。对肺癌病人及非病人吸烟、GSTM1基因缺失因素进行叉生分析,吸烟与GSTM1基因缺失对肺癌发生的危险有协同作用。结论GSTM1基因可作为肺癌遗传易感性标志物。

GSTM1基因多态性及启动子甲基化在结肠癌细胞系中的研究

目的研究参与内毒物代谢的重要酶谷胱甘肽-S-转移酶M1(glutathione-s-transferase M1,GSTM1)在结肠癌细胞系中的基因表达状况与其遗传基因型及启动子甲基化的关系。方法采用多重PCR方法检测GSTM1基因型,甲基化特异PCR(MSP)方法检测GSTM1基因启动子甲基化状态;用5-aza-dC处理结肠癌细胞系,RT-PCR方法检测GSTM1基因转录水平。结果结肠癌细胞系HT29、SW480、SW1116为GSTM1非空白基因型,而HCT116、Lovo、Colo结肠癌细胞系为GSTM1空白基因型。MSP检测发现SW1116细胞中GSTM1基因主要呈非甲基化状态,其他5个细胞系中呈甲基化状态,而且基因表达缺失。经5-aza-dC处理后,HT29和SW480细胞的GSTM1基因表达复活,而HCT116、Lovo、Colo细胞中GSTM1仍无扩增。结论 GSTM1基因转录受到遗传基因型和表观遗传启动子甲基化双重调控。

云南籍正常人群和肺癌人群GSTM1基因型多态性的比较研究

实验采用聚合酶链式反应 ( Polymerase Chain Reaction,PCR)技术对云南籍正常人群和肺癌人群的 GSTM1基因型多态性进行了检测。GSTM1基因纯合缺失 ( GSTM1 0 /0 )在正常人群中的分布频率为 65 .8% ( n =99) ,而在肺癌人群中分布频率为 76.8% ( n =5 6)。结果表明 GSTM1基因型多态性在云南籍正常人群和肺癌人群中的分布频率无显著性差异。

Anticancer Drug Resistance of HeLa Cells Transfected With Rat Glutathione S-transferase pi Gene

To establish a cytologic expressing system of rat glutathione S-transferase pi (GST-pi) cDNA for detecting the resistance of HeLa cells to anticancer drugs. Methods The assessment was made with various anticancer drugs (adriamycin, mitomycin, cisplatinum and vincristine) that showed different cytotoxicities in transfectant HeLa cells with pSV-GT containing rat GST-pi cDNA (HeLa/pSV-GT) or control pSV-neo (HeLa/pSV-neo). Expression levels of GST-pi mRNA in HeLa/pSV-GT and HeLa/pSV-neo were measured by in situ hybridization using Digoxin-labelled cDNA probe. Results HeLa/pSV-GT expressed significantly high degree of GST-pi mRNA, whereas both HeLa/pSV-neo and HeLa cells had very low expression. Cytotoxicities of HeLa/pSV-GT and HeLa/pSV-neo with 4 anticancer drugs were measured by MTT assay. Drug concentrations for yielding 50% inhibition (IC50) in HeLa/pSV-GT by adriamycin, mitomycin and cisplatinum were 70.13 靏/mL, 10.95 靏/mL and 16.52 靏/mL, respectively. In contrast, IC50 in HeLa/pSV-neo was 10.34 靏/mL, 7.48 靏/mL and 13.70 靏/mL, respectively. The cytotoxicities of vincristine on both HeLa/pSV-GT and HeLa/pSV-neo were not significantly different. Conclusions Our findings suggest that HeLa/pSV-GT containing rat GST-pi cDNA is resistant to some anticancer drugs due to overexpression of GST-pi. Also, HeLa/pSV-GT cell line could serve as a useful cytogenetic model for further research.

汉族人群谷胱甘肽-S-转移酶M1、T1基因多态性分析

目的 分析汉族人群谷胱甘肽 -S -转移酶M 1、T1 (GSTM1、GSTT1 )的基因多态性分布。方法 样本为6 0名唐山地区汉族人群 ,采用多重等位基因聚合酶链反应 (PCR)方法分析GSTM 1和GSTT1基因多态性。结果 GSTM1缺失型和GSTT1缺失基因型频率分别为 33 3%和 1 1 7% ,同时具有GSTM1缺失型和GSTT1缺失型的个体频率为 1 7%。结论 唐山地区GSTM 1、GSTT1基因呈多态性分布 ,其等位基因和基因型频率不同于其他种族。

抗氧化酶过表达对趋磁螺菌MSR-1耐氧性的影响

在格瑞斯瓦尔德磁螺菌(Magnetospirillum gryphiswa ldense)MSR-1中分别过量表达3种抗氧化酶Fe-超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶HPII,并分析过量表达这3种酶对趋磁螺菌MSR-1耐氧性的影响。通过PCR分别扩增大肠杆菌DH5α的Fe-超氧化物歧化酶(sodB)、谷胱甘肽过氧化物酶(btuE)、过氧化氢酶HPⅡ(katE)基因序列,将前两个片段分别连接到广宿主质粒pBBR1MCS-2上,后一个片段连接到广宿主质粒pBBR1MCS-5上,构建成表达质粒pBBR1MCS-sodB,pBBR1MCS-btuE和pBBR1MCS-katE,将3个质粒通过双亲接合转移的方法分别转入趋磁螺菌MSR-1。3种抗氧化酶过表达对趋磁螺菌MSR-1耐氧性影响的试验结果为过量表达Fe-超氧化物歧化酶对菌体生长影响不明显;过量表达谷胱甘肽过氧化物酶、过氧化氢酶HPII使趋磁螺菌MSR-1致死。上述试验结果表明抗氧化酶系在菌体耐氧过程中的全局协调调控的重要性。