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urinary bladder neoplasms/glutathione
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Erythrocyte glutathione and its metabolizing enzymes in bovine urinary bladder cancer.
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Glutathione and its metabolizing enzymes were studied in erythrocytes of cattle suffering from urinary bladder cancer and associated hematuria. The concentration of glutathione (GSH) and GSH peroxidase activity were subnormal in the affected animals, whereas activities of GSH reductase and GSH
Glutathione S-Transferase Pi 1 (GSTP1) Gene 313 A/G (rs1695) polymorphism is associated with the risk of urinary bladder cancer: Evidence from a systematic review and meta-analysis based on 34 case-control studies.
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Glutathione S-transferases in kidney and urinary bladder tumors.
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Exposure to potential carcinogens is an etiologic factor for renal cell carcinoma (RCC) and transitional cell carcinoma (TCC) of the urinary bladder. Cytosolic glutathione S-transferases (GSTs) are a superfamily of enzymes that protect normal cells by catalyzing conjugation reactions of
Low activities of glutathione-related enzymes as factors in the genesis of urinary bladder cancer.
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A comparative study of reduced glutathione (GSH) concentrations and activities of GSH related-enzymes in urinary bladder transitional epithelium (UBTE), urinary bladder nontransitional tissue (UBNT), and liver of the rabbit, was carried out to investigate the reasons for the susceptibility of UBTE
[Effect of reduced glutathione on N-butyl-N-(4-hydroxybutyl)-nitrosamine-induced urinary bladder cancer in rats].
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Combined analysis of inherited polymorphisms in arylamine N-acetyltransferase 2, glutathione S-transferases M1 and T1, microsomal epoxide hydrolase, and cytochrome P450 enzymes as modulators of bladder cancer risk.
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Foreign compound-metabolizing enzymes may modify the risk of chemically induced cancer. We wanted to examine enzymes with putative relevance in urinary bladder cancer using molecular genetic analyses of heritably polymorphic enzymes. Arylamine N-acetyltransferase (NAT2); glutathione S-transferases
Genetic polymorphism of glutathione S-transferases M1 and T1 as a risk factor in lung and bladder cancers.
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A combined analysis of two polymorphic enzymes, glutathione S-transferase mu (GST M1) and q (GST T1) and their implication as cancer risk factors was performed in a case-control study of lung and bladder cancers. Using a multiplex polymerase chain reaction (PCR) based method, the frequency of the
Gene environment interaction in urinary bladder cancer with special reference to organochlorine pesticide: a case control study.
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Urinary bladder cancer (UBC) is a common disease worldwide with a higher incidence rate in developed countries. Organochlorine pesticides (OCPs), potent endocrine disrupters, are found to be associated with several cancers such as prostate, breast, bladder, etc. Glutathione S-transferase (GST) is a
Association between GSTM1 copy number, promoter variants and susceptibility to urinary bladder cancer.
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This study sought to determine the role of copy number variants (CNV) combined with other genetic variants in the Glutathione S-transferases Mu class1 (GSTM1) promoter in the development of urinary bladder cancer. TaqMan real-time PCR and direct sequencing were used to determine genetic variants.
Miners compensated for pneumoconiosis and glutathione s-transferases M1 and T1 genotypes.
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Chronic inhalation of quartz-containing dust produces reversible inflammatory changes in lungs resulting in irreversible fibrotic changes termed pneumoconiosis. Due to the inflammatory process in the lungs, highly reactive substances are released that may be detoxified by glutathione S-transferases.
Differential induction of reactive oxygen species through Erk1/2 and Nox-1 by FK228 for selective apoptosis of oncogenic H-Ras-expressing human urinary bladder cancer J82 cells.
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OBJECTIVE
This study sought to reveal mechanisms for differential regulation of reactive oxygen species (ROS) in histone deacetylase inhibitor FK228-induced selective apoptosis of oncogenic H-Ras-expressing human cancer cells.
METHODS
Human urinary bladder cancer J82 and oncogenic H-Ras-expressing
Isoenzyme-specific quantitative immunoassays for cytosolic glutathione transferases and measurement of the enzymes in blood plasma from cancer patients and in tumor cell lines.
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Enzyme-linked immunoassays (ELISAs) based on the double-antibody sandwich technique have been developed for the quantitative analysis of the major human cytosolic class Pi, Mu and Alpha glutathione transferases (GSTs). The procedures were optimized with respect to antibody concentration for coating
Glutathione S-transferase M1 and its variants A and B as host factors of bladder cancer susceptibility: a case-control study.
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Glutathione S-transferase M1 (GSTM1) is a foreign compound-metabolizing enzyme with a heritable complete lack of activity in about 50% of Caucasians. GSTM1 deficiency may predispose individuals to urinary bladder cancer. Thus, a hospital-based case-control study was performed with 296 patients with
Urinary bladder cancer risk factors in an area of former coal, iron, and steel industries in Germany.
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This study was performed to investigate the frequency of bladder cancer in patients with an occupational history such as underground hard coal mining and/or painting after the structural change in the local industry. A total of 206 patients with bladder cancer and 207 controls were enlisted
Diverse expression profiles of glutathione-S-transferase subunits in mammalian urinary bladders.
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The hGSTM1 null genotype has been associated with increased susceptibility to urinary bladder cancer. However, the extent to which the GSTM1 subunit actually contributes to GST activities in mammalian urinary bladders is not clear. For adult mice, urinary bladders exhibited GST activity which was
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