Evidence that human class Theta glutathione S-transferase T1-1 can catalyse the activation of dichloromethane, a liver and lung carcinogen in the mouse: Comparison of the tissue distribution of GST T1-1 with that of classes Alpha, Mu and Pi GST in human

Sherratt, Philip J.; Pulford, David; Harrison, David J.; Green, Trevor; Hayes, John D.

doi:10.1042/bj3260837

Cited by 136 publications

(90 citation statements)

References 58 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…44 Although GST enzymes generally lead to conjugation and elimination of carcinogenic and toxic metabolites, some instances have been reported where GSTT leads to carcinogen activation. 45 Finally, it is also possible that GSTT could catalyze the conjugation and removal of anticarcinogenic components of the diet such as isothiocyanates, so deletion of the gene would be protective in certain circumstances. 46,47 Even when the potential combined effect of GSTM1 null, GSTT1 null and NAT2 slow genotypes was examined, no evidence of an interaction between these polymorphisms was observed.…”

Section: Discussionmentioning

confidence: 99%

N‐Acetyltransferase‐2, glutathione S‐transferase M1 and T1 genetic polymorphisms, cigarette smoking and hepatocellular carcinoma: A case‐control study

Gelatti

Covolo

Talamini

et al. 2005

Intl Journal of Cancer

View full text Add to dashboard Cite

Our aim was to evaluate the role of N-acetyltransferase (NAT2) and glutathione S-transferase M1 and T1 (GSTM1 and GSTT1) polymorphisms in hepatocellular carcinoma (HCC) according to cigarette smoking, taking into account hepatitis B (HBV) and C (HCV) viral infection as well as alcohol consumption. A hospitalbased case-control study was conducted in 2 areas of north Italy. Cases (n = 200) were patients hospitalized for HCC, and controls (n = 400) were patients admitted for reasons other than liver disease, neoplasms and tobacco-and alcohol-related diseases. Genotypes were determined using PCR and the PCR/restriction fragment length polymorphism-based method. The putative risk genotypes NAT2 slow acetylator, GSTM1 null and GSTT1 null were not associated with HCC (OR = 1.3, 95% CI 0.8-2.0; OR = 1.0, 95% CI 0.6-1.5; OR = 0.8, 95% CI 0.4-1.4, respectively). Although not statistically significant, an increase in HCC risk was observed among light smokers (1-20 pack-years) carrying GSTT1 null (OR = 1.7, 95% CI 0.6-4.7) and NAT2 slow acetylator (OR = 1.3, 95% CI 0.6-3.0) genotypes. In conclusion, there was no evidence for a gene-environment interaction in HCC risk for GSTM1, GSTT1 and NAT2 genotypes. ' 2005 Wiley-Liss, Inc.

show abstract

Section: Discussionmentioning

confidence: 99%

N‐Acetyltransferase‐2, glutathione S‐transferase M1 and T1 genetic polymorphisms, cigarette smoking and hepatocellular carcinoma: A case‐control study

Gelatti

Covolo

Talamini

et al. 2005

Intl Journal of Cancer

View full text Add to dashboard Cite

show abstract

“…Unfortunately attempts in multiple laboratories to demonstrate glutathione S-transferase enzyme activity for Ure2 have been unsuccessful (7,16,20). Although negative results are rarely reported in detail, the lack of success might derive from inherent instability in the enzyme, an observed characteristic of glutathione S-transferases, or from performing the assay with substrates that are not the preferred ones for the putative transferase (25)(26)(27)(28). The difficulties experienced in attempts to assay an enzyme activity prompted us to take a step backward from in vitro assays and ask more simply whether Ure2 is required for protection of cells against the growth-inhibitory effects of compounds reported to be glutathione S-transferase substrates in other organisms.…”

Section: Ure2 Is Required For Protection Against Heavy Metals-ure2mentioning

confidence: 99%

Ure2, a Prion Precursor with Homology to Glutathione S-Transferase, Protects Saccharomyces cerevisiae Cells from Heavy Metal Ion and Oxidant Toxicity

Rai

Tate

Cooper

2003

Journal of Biological Chemistry

View full text Add to dashboard Cite

Ure2, the protein that negatively regulates GATA factor (Gln3, Gat1)-mediated transcription in Saccharomyces cerevisiae, possesses prion-like characteristics. Identification of metabolic and environmental factors that influence prion formation as well as any activities that prions or prion precursors may possess are important to understanding them and developing treatment strategies for the diseases in which they participate. Ure2 exhibits primary sequence and three-dimensional homologies to known glutathione S-transferases. However, multiple attempts over nearly 2 decades to demonstrate Ure2-mediated S-transferase activity have been unsuccessful, leading to the possibility that Ure2 may well not participate in glutathionation reactions. Here we show that Ure2 is required for detoxification of glutathione S-transferase substrates and cellular oxidants. ure2⌬ mutants are hypersensitive to cadmium and nickel ions and hydrogen peroxide. They are only slightly hypersensitive to diamide, which is nitrogen source-dependent, and minimally if at all hypersensitive to 1-chloro-2,4-dinitrobenzene, the most commonly used substrate for glutathione S-transferase enzyme assays. Therefore, Ure2 shares not only structural homology with various glutathione S-transferases, but ure2 mutations possess the same phenotypes as mutations in known S. cerevisiae and Schizosaccharomyces pombe glutathione S-transferase genes. These findings are consistent with Ure2 serving as a glutathione S-transferase in S. cerevisiae.Several neurodegenerative conditions derive from the same pathogenetic mechanism, i.e. a change in protein conformation, polymerization, and plaque formation. These conditions have been called conformational diseases such as Alzheimer's and the prionoses. Recent studies have demonstrated that a protein associated with such disease, amyloid ␤-protein, protects neurons from metal-induced oxidative damage (1). Neither the molecular basis for this activity nor how it is affected by environment and neuronal metabolism is yet known. The use of eukaryotic model systems, such as the yeast Saccharomyces cerevisiae, has greatly facilitated our acquisition of information about mammalian proteins, their functions and interactions, and how their synthesis and activities are regulated and integrated. In particular, the genetic study of prions has been

show abstract

“…25,[52][53][54] These findings are not surprising, since, although GSTs are generally recognized as detoxifying enzymes, they could also be involved in the generation and activation of toxic compounds. 55,56 Recent evidences support the role of bioactivation by GSTs. 57 …”

Section: Assessment Of the Role Of Selected Gst Genes Towards Susceptmentioning

confidence: 99%

Cytogenetic damage and genetic variants in the individuals susceptible to arsenic‐induced cancer through drinking water

Ghosh

Basu

Mahata

et al. 2006

Intl Journal of Cancer

113

View full text Add to dashboard Cite

In West Bengal, India, more than 300,000 arsenic-exposed people are showing symptoms of arsenic toxicity, which include cancers of skin and different internal organs. Since only 15-20% of the exposed population manifest arsenic-induced skin lesions, it is thought that genetic variation might play an important role in arsenic toxicity and carcinogenicity. A total of 422 unrelated arsenic-exposed subjects (244 skin-symptomatic and 178 asymptomatic) were recruited for this study. Cytogenetic damage, as measured by chromosomal aberrations in lymphocytes and micronuclei formation in oral mucosa cells, urothelial cells and binucleated lymphocytes, was studied in unexposed, skin-symptomatic and asymptomatic individuals with similar socioeconomic status. Identification of null mutations in GSTT1 and GSTM1 genes were carried out by PCR amplification. GSTP1 SNPs, implicated in susceptibility to various cancers, were assessed by PCR-RFLP method. Symptomatic individuals had higher level of cytogenetic damage compared to asymptomatic individuals and asymptomatic individuals had significantly higher genotoxicity than unexposed individuals. No difference in allelic variants in GSTT1 and GSTP1 was observed between these 2 groups. Incidence of GSTM1 null gene frequencies was significantly higher in the asymptomatic group. Individuals with GSTM1-positive (at least one allele) had significantly higher risk of arsenic-induced skin lesions (odds ratio, 1.73; 95% confidence interval, 1.24-2.22). These results show a protective role of GSTM1 null in arsenic toxicity. This study also indicates that asymptomatic individuals are sub clinically affected and are also significantly susceptible to arsenicinduced genotoxicity. ' 2005 Wiley-Liss, Inc.

show abstract

Evidence that human class Theta glutathione S-transferase T1-1 can catalyse the activation of dichloromethane, a liver and lung carcinogen in the mouse: Comparison of the tissue distribution of GST T1-1 with that of classes Alpha, Mu and Pi GST in human

Cited by 136 publications

References 58 publications

N‐Acetyltransferase‐2, glutathione S‐transferase M1 and T1 genetic polymorphisms, cigarette smoking and hepatocellular carcinoma: A case‐control study

N‐Acetyltransferase‐2, glutathione S‐transferase M1 and T1 genetic polymorphisms, cigarette smoking and hepatocellular carcinoma: A case‐control study

Ure2, a Prion Precursor with Homology to Glutathione S-Transferase, Protects Saccharomyces cerevisiae Cells from Heavy Metal Ion and Oxidant Toxicity

Cytogenetic damage and genetic variants in the individuals susceptible to arsenic‐induced cancer through drinking water

Contact Info

Product

Resources

About