Glutathione S-transferase T1 Polymorphisms Research Articles

An updating meta-analysis of the glutathione S-transferase T1 polymorphisms and colorectal cancer risk: a HuGE review

GSTT1 status has been extensively studied as a colorectal cancer risk factor. However, the results are inconsistent. To examine this controversy, we performed a meta-analysis to evaluate the relationship between GSTT1 polymorphism and colorectal cancer. We performed a literature search using PUBMED, EMBASE, Cochrane Library, and HuGNet database to February 2009, with no restrictions. All articles were independent and contained the minimum information necessary to estimate the colorectal cancer risk associated with GSTT1 null. Summary odds ratio (ORs) and 95% confidence intervals (CIs) were calculated using random-effect or fixed-effect models based on the heterogeneity of included studies. A total of 23 case-control studies, including a total of 11,057 subjects (5,058 cases and 5,999 controls), that related to GSTT1 polymorphism and risk of colorectal cancer were identified and included for analysis. The random-effect meta-analyses of all the 23 studies suggested that there was a small increased risk of colorectal cancer for individuals with GSTT1 null (OR was 1.23; 95% CI 1.02-1.49; I (2) = 76.9%, P for heterogeneity <0.001). The fixed-effect meta-analyses reached a similar results in Caucasians populations of ten studies (OR = 1.39; 95% CI 1.21-1.59; I (2) = 29.8%, P for heterogeneity = 0.171) and Asians populations of five studies (OR = 1.23; 95% CI 1.04-1.45; I (2) = 0.0%, P for heterogeneity = 0.428), with as inversely association in the other ethnic populations from four studies (OR = 0.69; 95% CI 0.54-0.877; I (2) = 0.0%, P for heterogeneity = 0.58). There was a small increased risk of colorectal cancer for individuals with GSTT1 null, especially for Caucasians populations and Asian populations.

Genetic polymorphisms of glutathione S-transferase T1 and bladder cancer risk: a meta-analysis

In recent years, there have been numerous papers emphasizing the relationship between Glutathione S-transferases polymorphisms and bladder cancer risk, but the findings have not reached a consensus. The relationship between glutathione S-transferase T 1 null genotype and bladder cancer susceptibility is now even more disputable. Therefore, we present a meta-analysis of (nested) case-controlled, genotype-based studies (including 37 studies, 6,986 cases and 9,166 controls) examining this association. Using a fixed-effect model, statistically significant increase was observed between glutathione S-transferase T 1 deletion and bladder cancer risk for the overall studies (OR = 1.12; 95% confidence interval (CI): 1.04-1.21; P = 0.004 for Z test; I (2) = 47.43 for heterogeneity). After adjusting the result using trim-and-fill method, the outcome still had significant difference with little downgrade (OR = 1.10, 95% CI = 1.02-1.18). Three potential sources of heterogeneity including ethnicity, source of control and smoking status were also assessed. Minor increased correlation was found only in population-based studies (OR = 1.16; 95% CI = 1.03-1.30; I (2) = 47.16). Our analysis suggests that glutathione S-transferase T 1 null status is associated with a modest increase in the risk of bladder cancer and the difference exiting in source of control has been confirmed. Due to limited sample size, various confounding variables as well as discrepancy in study design, a valid conclusion still cannot be confirmed.

The Role of Glutathione S-Transferases in Urinary Tract Tumors

The Role of Glutathione S-Transferases in Urinary Tract Tumors Exposure to potential carcinogens is among the etiological factors for renal cell carcinoma (RCC) and transitional cell carcinoma (TCC) of the urinary bladder. RCC is very resistant, while TCC exhibits a high recurrence rate and multifocality. Cytosolic glutathione S-transferases (GST) are a superfamily of enzymes which protect normal cells by catalyzing conjugation reactions between electrophylic compounds, including carcinogens, and glutathione. Some GST enzymes posses hydroperoxidase activity. The most well characterized classes have been named Alpha (GSTA), Mu (GSTM), Pi (GSTP) and Theta (GSTT) and each of these classes contains several different isoenzymes. Several types of allelic variation have been identified within classes, among which GSTM1-null and GSTT1-null confer impaired catalytic activity. Individuals with the GSTM1-null genotype carry a substantially higher risk for bladder carcinogenesis. The effects of glutathione S-transferase T1 polymorphism on the increased susceptibility to RCC and TCC of urinary bladder depend on the presence of specific chemical exposures to compounds metabolized via the GSTT1-1 pathway. In the process of kidney cancerisation expression of GST alpha isoenzymes tends to decrease, consequently favoring a prooxidant environment necessary for the growth of RCC. GST pi enzyme activities are generally retained in RCC and might contribute to the chemotherapy resistance of RCC. In the malignant phenotype of TCC of the urinary bladder up regulation of various GST classes occurs. Up regulation of GSTT1-1 and GSTP1-1 might have important consequences on the tumor growth, by providing a reduced environment and inhibition of apoptotic pathways.

Placental Anti-Oxidant Gene Polymorphisms, Enzyme Activity, and Oxidative Stress in Preeclampsia

The etiology and pathophysiology of preeclampsia are not fully understood. However, oxidative stress has been strongly linked to the occurrence of this multi-system disease. This has led to many theories of the pathogenesis of preeclampsia involving placental oxidative stress. In this study, we hypothesized that polymorphisms of anti-oxidant genes in the placental tissue contributed to susceptibility to preeclampsia. Polymorphisms in copper/zinc superoxide dismutase (CuZn-SOD), manganese superoxide dismutase (MnSOD), glutathione- S-transferase M1 (GSTM1), and glutathione- S-transferase T1 (GSTT1) in the umbilical cord tissue were assayed by polymerase chain reaction (PCR) in 23 nulliparous preeclampsia cases and 32 nulliparous normotensive controls. Corresponding enzyme activity levels and an oxidative stress biomarker (8-isoprostane) of the placental tissue were also measured. In addition, maternal plasma 8-isoprostane levels were also determined. Our results showed that no significant differences in polymorphism frequency of the tested genes, enzyme activity levels or 8-isoprostane levels in the placental tissue were detected between the cases and controls. However, maternal plasma 8-isoprostane level was significantly higher in the cases than in the controls (105.8 vs. 27.9 pg/ml, p = 0.03). In conclusion, our study showed that polymorphisms of CuZn-SOD, MnSOD, GSTM1 and GSTT1 in the placental tissue were not associated with preeclampsia.

An association study of sodium-lithium countertransport activity with glutathione S transferase (GST) T1 and GST M1 null polymorphisms in Greek dyslipidaemic patients and controls

Previous genomic linkage studies have produced evidence linking sodium-lithium countertransport activity (Na/Li CT) with various chromosomal regions including loci harbouring glutathione S transferase (GST) genes. The aim of this study was to examine the putative association of erythrocyte Na/Li CT activity with GST T1 and M1 gene null polymorphisms. Na/Li CT activity was determined in erythrocytes isolated from 85 individuals, using a standard assay procedure employing atomic absorption spectroscopy. Genotyping of the GST T1 and GST M1 null polymorphisms was accomplished with a multiplex PCR method. A general linear model using age, sex, smoking, dyslipidaemia and hypertension as covariates was used to examine the association of Na/Li CT activity with the GST T1 and GST M1 genotypes. Individuals with the GST T1 null genotype displayed marginally significantly (p=0.049) lower values of Na/Li CT activity compared to those harbouring at least one copy of the GST T1 gene. The significance of this association was eliminated following adjustment for covariates (p=0.150), but survived as a trend when the sample was limited to normotensive and normolipidaemic individuals (p=0.070). No association was detected between the GST M1 null polymorphism and Na/Li CT activity. The suggestive association of the GST T1 null polymorphism with erythrocyte Na/Li CT activity is in line with previously published data from genetic linkage and biochemical analyses and may be of potential prognostic value as regards the behaviour of the countertransport and the development of related pathologies under conditions of oxidative insult.

Influence of polymorphism of glutathione S-transferase T1 on Chinese infertile patients with varicocele

To investigate the influence of glutathione S-transferase T1 (GSTT1) gene polymorphism on Chinese infertile patients with varicocele, 63 infertile patients with varicocele and 54 healthy fertile controls were recruited in this case-control study. Our results show that oxidative damage may be the cause of infertility in patients with varicocele, and GSTT1 null genotype predisposes to over oxidative damage to spermatocytes of infertile patients with varicocele.

Genetic Polymorphism of Glutathione S-transferase T1, M1 and Asthma, A Meta-analysis of the Literature

Published studies have confirming or refusing an association between either glutathione S-transferase T1 (GSTT1) or M1 (GSTM1) polymorphism and asthma risk. Therefore the present meta-analysis was done. Literature-based meta-analysis was supplemented by tabular data from investigators of all relevant studies of two GST polymorphism (GSTM1 and GSTT1) available before May 2006, with investigation of potential sources of heterogeneity. Included in the resent study were 14 studies, involving a total 2292 asthma patients and 5718 controls. We found substantial evidence of heterogeneity between the studies. Exclusion of two studies with lowest quality scores resulted in a dramatic decrease in heterogeneity. The overall OR of the asthma risk associated with GSTM1 null genotype was 1.20 (95% CI: 1.08-1.35). Stratifying the meta-analysis by age and smoking status of subjects, the pooled ORs for GSTM1 null genotype were 1.56 (95% CI: 1.25-1.94) in adults and 1.95 (95% CI: 1.21-3.13) in non-smokers. The GSTT1 null genotype was associated with asthma risk in non-smoker adults (OR = 2.06, 95% CI: 1.21-3.71). To investigate whether profile of GST genotypes are associated with the risk of the asthma, further analysis combining the GSTT1 and GSTM1 genotypes were also carried out. Subjects with null genotypes for both GSTM1 and GSTT1 were at a significant higher risk for developing asthma (OR = 2.15, 95% CI: 1.39-3.33) compared with subjects who had both active genes. The trend in risk associated with zero, one and two putative high-risk genotypes was significant (chi2 = 12.07, df= 1, p = 0.0005). Overall, our present meta-analysis revealed that the null genotypes of GSTM1 and GSTT1 are associated with risk of asthma in adults especially in non-smoker ones. It might be suggested that chronic smoking carries such a high dose of toxins into the body that overloads the capacity of either GSTM1 or GSTT1 detoxification system. It seems that the GSTM1 and GSTT1 lack their protective values against development of asthma in adults with positive history of smoking. Present results also suggested that there is an additive effect for GSTT1 and GSTM1 genotypes.

Genetic polymorphisms of glutathione S-transferase T1 ( GSTT1) and alterations of sex hormones in filling-station workers

To determine the health effects of gasoline exposure as measured by levels of sex hormones (total testosterone, follicle-stimulating hormone [FSH], and luteinizing hormone [LH]) of male filling-station workers. Case-control study. Filling stations in Shiraz (Fars province, Iran). One hundred fourteen male gasoline workers and 112 age-matched (+/-5 years) and sex-matched controls with no occupational exposure to gasoline. None. Serum levels of testosterone, FSH, and LH, and expression of the GSTT1 genotype. All hormone measurements were in the normal range although subclinical changes were detected in some indexes. Men exposed to petrochemicals had lower mean serum testosterone levels compared with unexposed men, regardless of the presence of the GSTT1 genotype. However, this decrease (expressed as mean +/- standard deviation) is most pronounced in the group possessing the GSTT1-null genotype (4.26 +/- 1.44 ng/mL vs. 5.48 +/- 0.98 ng/mL) compared with the group possessing the GSTT1 genotype (4.23 +/- 1.73 ng/mL vs. 4.67 +/- 1.21 ng/mL). The LH levels varied between the two groups; the mean serum LH was lower in the exposed versus unexposed men who possessed the GSTT1 genotype (2.82 +/- 1.32 IU/L vs. 3.20 +/- 1.17 IU/L) and higher in the exposed versus unexposed men who possessed the GSTT1-null genotype (3.52 +/- 1.37 IU/L vs. 2.76 +/- 1.07 IU/L). Testosterone levels were statistically significantly decreased in male gasoline workers compared with men who had had no occupational exposure to gasoline. The relevance of the GSTT1 genotype to these differences remains to be determined.

Glutathione S-transferase T1 (GSTT1) and M1 (GSTM1) polymorphisms in a sample of the population in Northern Italy

Glutathione S-transferase is a group of multifunctional enzymes important in the metabolism of xenobiotics. GSTT1 and GSTM1 are polymorphic in human populations. Since a relation between polymorphism and cancer susceptibility has been found, their distribution in human populations is of great interest. In the present study the distribution of GSTT1 and GSTM1 genotypes was studied in a total sample of 252 individuals of three localities of north-west Italy (Postua, Cavaglià and Biella) by PCR test. The frequencies of GSTT1 and GSTM1 "null" genotypes were respectively 7.94% and 34.92%. There are no significant differences between the populations studied in the GSTT1 "null" genotypes. On the other hand, for GSTM1 the frequency of gene deletion in Postua (25.5%) differs significantly (p < 0.01; chi-square test) from that of Biella (46.32%), which approaches the values indicated by most studies for Europeans (about 50%). The analysis of the frequencies of GSTT1 and GSTM1 polymorphisms among different age groups showed a lower frequency of negative genotypes in the older group, although not statistically confirmed.

Association between susceptibility to advanced stage endometriosis and the genetic polymorphisms of aryl hydrocarbon receptor repressor and glutathione-S-transferase T1 genes

This study was performed to determine whether genetic polymorphisms of aryl hydrocarbon receptor repressor (AhRR), glutathione-S-transferase M1 (GSTM1) and glutathione-S-transferase T1 (GSTT1) are associated with susceptibility to advanced stage endometriosis in a Korean population. This study comprised 316 women with advanced stage endometriosis and 256 control women without endometriosis. Genotyping of the AhRR codon 185 was performed by real-time polymerase chain reaction (PCR) analysis. GSTM1 and GSTT1 genotyping for gene deletions were carried out by multiplex PCR analysis. G allele frequency at codon 185 of AhRR was increased in patients with endometriosis (P=0.047), and there was a trend for an association of C/G+G/G genotypes with risk of endometriosis (P=0.06). The proportion of null mutation at GSTT1 also tended to increase (P=0.06) in patients with endometriosis, whereas there was no difference in the genotype distribution of GSTM1 genes. Analyzing AhRR and GSTT1 together, we found that patients with high-risk genotypes at both loci have increased risk of endometriosis, compared with patients without high-risk genotypes (P=0.015). These findings suggest that the AhRR codon 185 and GSTT1 polymorphisms are associated with the risk of advanced stage endometriosis.

P058 Polymorphisms of glutathione S-transferase T1 and M1 in Greek patients with myelodysplastic syndrome in relation to patient characteristics and cytogenetic subgroups

P058 Polymorphisms of glutathione S-transferase T1 and M1 in Greek patients with myelodysplastic syndrome in relation to patient characteristics and cytogenetic subgroups

Expression of glutathione S-transferase T1 (GSTT1) in human brain tumours.

Glutathione S-transferases (GSTs) play a central role in a number of metabolic processes. Glutathione S-transferase T1 (GSTT1) is a polymorphic cytosolic enzyme and a member of the theta class of GSTs. Typical substrates for GSTT1 are industrial compounds, such as dichloromethane and ethylene oxide. It has been shown that also chemotherapeutic drugs such as BCNU [i.e. 1,3-bis(2-chloroethyl)-1-nitrosourea] are efficiently inactivated by GSTT1. BCNU is a drug which is increasingly used locally in the chemotherapy of glioblastoma multiforme WHO grade IV. Therefore, if GSTT1 were expressed in neoplastic cells of brain tumours it could be a factor for chemoresistance. In order to clarify a possible role of GSTT1 in chemoresistance, as a first step, we localized this enzyme in malignant gliomas such as glioblastoma multiforme WHO grade IV and oligodendroglioma WHO grade II. Because of its polymorphism we first genotyped the samples for GSTT1 by PCR. Using in situ hybridization, we then demonstrated that GSTT1 transcripts are expressed in neoplastic cells of both tumour types. Immunohistochemistry revealed then that whereas neoplastic cells in glioblastoma multiforme WHO grade IV contain GSTT1, it was not localized in oligodendroglioma cells. Given the polymorphism of GSTT1 and its potential activity towards BCNU, the localization of GSTT1 in glioblastoma cells can be considered as a possible factor of non-homogeneous chemotherapy response among patients with different GSTT1 genotypes.

Genetic polymorphisms of glutathione S‐transferase T1 (GSTT1) and susceptibility to gastric cancer: a meta‐analysis

The association between glutathione S-transferase T1 (GSTT1) polymorphism and gastric cancer risk has been both confirmed and refuted in a number of published studies. Most of these studies were based on small sample sizes. We carried out a meta-analysis of the research published up to August 2005 to obtain more precise estimates of gastric cancer risk associated with GSTT1 polymorphism. In the present study, 16 case-control studies (with a total of 6717 subjects) were eligible for meta-analysis. There was no evidence of heterogeneity between the studies. The GSTT1 null genotype conferred a 1.06-fold increased risk of gastric cancer, which was not significant (95% confidence interval [CI]: 0.94-1.19). However, in the analysis of ethnic groups, we observed distinct differences associated with GSTT1 status. Restricting analyses to ethnic groups, the pooled odd ratios for the GSTT1 genotype were 1.27 in Caucasians (95% CI: 1.03-1.57) and 0.98 in Asians (95% CI: 0.86-1.13). Glutathione S-transferase M1 (GSTM1) and GSTT1 are involved in detoxification of a variety of compounds, some that overlap between enzymes and some that are highly specific. To investigate whether the profile of glutathione S-transferase genotypes was associated with risk of gastric cancer, further analyses combining the GSTT1 and GSTM1 genotypes were also carried out. There was a significant trend in risk associated with zero, one and two putative high-risk genotypes (chi2 = 9.326, d.f. = 1, P = 0.0023). Those who had null genotypes of GSTM1 and GSTT1 had an increased gastric cancer risk compared with those who had both active genes (odds ratio = 2.08, 95% CI: 1.42-3.10).

Exploring SNP‐SNP interactions and colon cancer risk using polymorphism interaction analysis

Several single nucleotide polymorphisms (SNPs) in genes derived from distinct pathways are associated with colon cancer risk; however, few studies have examined SNP-SNP interactions concurrently. We explored the association between colon cancer and 94 SNPs, using a novel approach, polymorphism interaction analysis (PIA). We developed PIA to examine all possible SNP combinations, based on the 94 SNPs studied in 216 male colon cancer cases and 255 male controls, employing 2 separate functions that cross-validate and minimize false-positive results in the evaluation of SNP combinations to predict colon cancer risk. PIA identified previously described null polymorphisms in glutathione-S-transferase T1 (GSTT1) as the best predictor of colon cancer among the studied SNPs, and also identified novel polymorphisms in the inflammation and hormone metabolism pathways that singly or jointly predict cancer risk. PIA identified SNPs that may interact with the GSTT1 polymorphism, including coding polymorphisms in TP53 (Arg72Pro in p53) and CASP8 (Asp302His in caspase 8), which may modify the association between this polymorphism and colon cancer. This was confirmed by logistic regression, as the GSTT1 null polymorphism in combination with either the TP53 or the CASP8 polymorphism significantly alter colon cancer risk (p(interaction) < 0.02 for both). GSTT1 prevents DNA damage by detoxifying mutagenic compounds, while the p53 protein facilitates repair of DNA damage and induces apoptosis, and caspase 8 is activated in p53-mediated apoptosis. Our results suggest that PIA is a valid method for suggesting SNP-SNP interactions that may be validated in future studies, using more traditional statistical methods on different datasets.

Genetic polymorphisms of GSTT1, GSTM1, and NQO1 genes and diabetes mellitus risk in Chinese population

Objective The aims of the present study were to assess whether the glutathione S-transferase T1 (GSTT1), M1 (GSTM1), and NAD(P)H: quinone oxidoreductase 1 (NQO1) genotypes are associated with type 2 diabetes mellitus (T2 DM) and to ascertain whether the levels of blood lipids given exposure to diabetes are modified by the specific genetic polymorphisms of GSTT1, GSTM1, and NQO1. Methods This case-control study was conducted on 200 subjects. The genotypes were determined using a polymerase chain reaction (PCR) and PCR-restriction fragment length polymorphism. Results The GSTT1-present genotype conferred a statistically significant 0.49-fold reduction in risk of T2 DM relative to the null genotype. Individuals with GSTT1-null or GSTM1-null genotype had higher levels of low-density-lipoprotein cholesterol, apolipoprotein B, and lipoprotein(a), respectively. There was no association between either GSTM1 or NQO1 polymorphism and risk of T2 DM. Conclusion The present results suggest that the GSTT1 gene may contribute to the development of T2 DM and may be one of the candidate genes of T2 DM in Chinese population.

Analysis of glutathione and vitamin C effects

The alkaline single-cell gel electrophoresis (or Comet) assay was applied to evaluate the eventual DNA damage induced by the triphenolic metabolite of benzene, 1,2,4-benzenetriol (BT), in isolated human lymphocytes. Prior to BT treatment, ranging from 5 to 50 μM, a supplementation with glutathione (GSH, 350 μg/ml) was carried out to assess whether GSH may have a modulating effect on the Comet response. The effect of a fixed dose of BT was also evaluated in the presence of the exogenous antioxidant vitamin C (40 and 200 μM). Additionally, we investigated whether the polymorphism of glutathione S-transferase T1 (GSTT1) gene may affect the individual level of BT-induced DNA damage in vitro. For all donors included in the present study, BT produced a significant dose-response relationship. No clear effect of GSH preincubation was seen on the BT-induced response. On the contrary, a significant reduction of DNA damage was observed in the presence of vitamin C (at least at 200 μM). Although our data suggest some individual differences according to the GSTT1 genotype in the outcome of the Comet assay, a large number of individuals should be studied in further investigations to obtain reliable conclusions.

No association of polymorphisms in the glutathione S‐transferase genes with pre‐eclampsia, eclampsia and HELLP syndrome in a Turkish population

There is substantial evidence that genetic factors play a role in pre-eclampsia. The aim of this study was to determine whether genetic variability in the encoding of genes for glutathione S-transferase M1 (GSTM1) and glutathione S-transferase T1 (GSTT1) contributes to individual differences in susceptibility to pre-eclampsia, eclampsia, or hemolysis, elevated liver enzymes, and low platelets (HELLP syndrome). A total of 221 women with pre-eclampsia, eclampsia and HELLP syndrome and 147 healthy female controls were genotyped for GSTM1 and GSTT1 polymorphisms by polymerase chain reaction (PCR). Statistical evaluation of differences in polymorphic rates was carried out using chi(2) analysis. This study included 140 pre-eclamptic, 33 eclamptic and 48 HELLP syndrome cases and 147 healthy controls. The frequencies for the GSTM1 null genotype were 58%, 45%, and 60% for pre-eclampsia, eclampsia, and HELLP syndrome, respectively, and in controls it was 55%. The distribution of the GSTT1 null genotype was 22%, 21%, and 27% for pre-eclampsia, eclampsia, and HELLP syndrome, respectively, and in controls it was 22%. There was no significant association between GSTM1 and GSTT1 polymorphisms and pre-eclampsia, eclampsia, and HELLP syndrome. Our data do not support a role for polymorphisms of the GSTM1 and GSTT1 genes in the pathogenesis of pre-eclampsia, eclampsia and HELLP syndrome.

Cigarette Smoking and Colorectal Cancer: APC Mutations, hMLH1 Expression, and GSTM1 and GSTT1 Polymorphisms

The contribution of cigarette smoking to sporadic colorectal cancer may differ according to molecular aspects of the tumor or according to glutathione S-transferase M1 (GSTM1) or glutathione S-transferase T1 (GSTT1) genotype. In the prospective Netherlands Cohort Study on Diet and Cancer, adjusted incidence rate ratios for 1986-1993 were computed for overall colorectal cancer, tumors with and without adenomatous polyposis coli (APC) mutations, and tumors with and without human mut-L homologue 1 (hMLH1) expression, according to cigarette smoking characteristics (661 cases, 2,948 subcohort members). Case-only analyses were performed to estimate odds ratios for interaction between cigarette smoking and GSTM1 and GSTT1 genotypes. In comparison with never smokers, a high smoking frequency increased the risk of colorectal cancer (for a five-cigarette/day increment, incidence rate ratio (IRR) = 1.07, 95% confidence interval (CI): 1.03, 1.12), and this association was stronger in 371 tumors without a truncating APC mutation (IRR = 1.11, 95% CI: 1.05, 1.17). Long-term smoking was associated with lack of hMLH1 expression in 56 tumors (for a 10-year increment, IRR = 1.17, 95% CI: 1.00, 1.37). No statistically significant interactions between smoking and GSTM1 or GSTT1 genotype were observed. These results indicate that cigarette smoking is associated with risk of colorectal cancer, and this association may depend on molecular characteristics of the tumor as defined by APC mutation and hMLH1 expression status.

Glutathione S-transferase M1, T1, and P1 gene polymorphism in laryngeal squamous cell carcinoma

Purpose To investigate the influence of the glutathione S-transferase (GST) M1, T1, and P1 genotypes on the laryngeal squamous cell carcinoma risk. Material and methods The study group consisted of 42 white patients with laryngeal squamous cell carcinoma (39 of them were male, mean age: 53, range: 37–67 and 3 of them were female, mean age: 47, range: 32–55) and 89 control subjects (nonsmokers = 47, smokers = 42) (58 male and 31 female, mean age: 51, range: 30–72). DNA samples were isolated from blood samples using high pure polymerase chain reaction (PCR) Template Preparation Kit. The detection of GST T1, GST M1, and P1 polymorphisms were detected by using real-time PCR. Results Gene polymorphisms at GST M1 and P1 were not significantly different in patient and control groups. However, GST T1 null type significantly increased in laryngeal cancer patients when compared with the nonsmoking controls ( P = .04). Conclusions There was a significant association between GST T1 null genotype and laryngeal squamous cell carcinoma. However the potential role of GSTs as markers of susceptibility to laryngeal carcinoma needs further studies in a larger number of patients.

Biological monitoring of workers exposed to dichloromethane, using head-space gas chromatography

A biological monitoring method for urinary dichloromethane (DCM) has been developed by using head-space gas chromatography with FID detection. The calibration curve is linear in a wide range of DCM levels between 0.01 and 2 mg/l. The recovery rate is almost 100% and within-run coefficients of variation are 2.9–3.7%. A highly significant correlation is found between exposure levels and urinary concentrations of DCM. Determination of urine DCM by this method has many advantages such as sample storage, no need for correction of urine concentration, absence of gender difference and also no confounding effect of glutathione S-transferase T1 polymorphism.