Abstract
The present study aimed to investigate the association between genetic polymorphisms of glutathione S-transferases (GSTs) and susceptibility to ulcerative colitis (UC) in central China. The prevalence of GSTM1, GSTT1, and GSTP1 gene polymorphisms were examined using polymerase chain reaction methods in 270 consecutive UC patients and 623 age- and sex-matched healthy controls. The frequencies of the GSTM1(null) and GSTT1(null) as well as GSTP1 (Val/Val) genotypes were significantly higher in UC patients than in the controls (70.74% vs. 41.74%, P = 0.0001; 64.82% vs. 47.19%, P = 0.0001; and 48.89% vs. 34.35%, P = 0.0004, respectively). When the UC patients were stratified according to clinical features, we found that the frequencies of the GSTT1(null) and GSTP1 (Val/Val) genotypes but not the GSTM1(null) genotype were significantly higher in patients with distal colitis than in extensive colitis (P = 0.0007, P = 0.001, and P = 0.271, respectively). However, these variant GST genotypes were not significantly linked to severity of the disease (P > 0.05). GST variant genotypes are strongly correlated with prevalence and extent but not with severity of UC in the Hubei Han population in central China.
Similar content being viewed by others
References
Andres, P. G., & Friedman, L. S. (1999). Epidemiology and the natural course of inflammatory bowel disease. Gastroenterology Clinics of North America, 28, 255–281.
Fiocchi, C. (1998). Inflammatory bowel disease: aetiology, pathogenesis. Gastroenterology, 115, 182–205.
Ogura, Y., Bonen, D. K., Inohara, N., et al. (2001). A frameshift mutation in NOD2 associated with susceptibility to Crohn’s disease. Nature, 411, 603–606.
Hugot, J. P., Chamaillard, M., Zouali, H., et al. (2001). Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn’s disease. Nature, 411, 599–603.
Tumer, Z., Croucher, P. J., Jensen, L. R., et al. (2002). Genomic structure, chromosome mapping and expression analysis of the human AVIL gene, and its exclusion as a candidate for locus for inflammatory bowel disease at 12q13–14 (IBD2). Gene, 288, 179–185.
Duerr, R. H., Taylor, K. D., Brant, S. R., et al. (2006). A genome-wide association study identifies IL23R as an inflammatory bowel disease gene. Science, 314, 1461–1463.
Van Limbergen, J., Russell, R. K., Nimmo, E. R., et al. (2007). Genetics of the innate immune response in inflammatory bowel disease. Inflammatory Bowel Diseases, 13, 338–355.
Young, Y., & Abreu, M. T. (2006). Advances in the pathogenesis of inflammatory bowel disease. Current Gastroenterology Reports, 8, 470–477.
Pemble, S., Schroeder, K. R., Spencer, S. R., et al. (1994). Human glutathione S-transferase u (GSTT1): cDNA cloning and the characterization of a genetic polymorphism. Biochemical Journal, 300, 271–276.
Seidegard, J., Pero, R. W., Markowitz, M. M., et al. (1990). Isoenzyme(s) of glutathione transferase (class Mu) as a marker for the susceptibility to lung cancer: a follow up study. Carcinogenesis, 11, 33–36.
Hu, X., Ji, X., Srivastava, S. K., et al. (1997). Mechanism of differential catalytic efficiency of two polymorphic forms of human glutathione S-transferase P1–1 in the glutathione conjugation of carcinogenic diol epoxide of chrysene. Archives of Biochemistry and Biophysics, 345, 32–38.
Sundberg, K., Johansson, A. S., Stenberg, G., et al. (1998). Differences in the catalytic efficiencies of allelic variants of glutathione transferase P1–1 towards carcinogenic diol epoxides of polycyclic aromatic hydrocarbons. Carcinogenesis, 19, 433–436.
Lennard-Jones, J. E. (1989). Classification of inflammatory bowel disease. Scandinavian Journal of Gastroenterology Supplement, 24, 2–6.
Truelove, S. C., & Witts, L. J. (1955). Cortisone in ulcerative colitis: final report on a therapeutic trial. British Medical Journal, 2, 1042–1048.
Curran, J. E., Weinstein, S. R., & Griffiths, L. R. (2000). Polymorphisms of glutathione transferase genes (GSTM1, GSTP1 and GSTT1) and breast cancer susceptibility. Cancer Letters, 153, 113–120.
Hirvonen, A. (1999). Polymorphisms of xenobiotic-metabolizing enzymes and susceptibility to cancer. Environmental Health Perspectives, 107(Suppl 1), 37–47.
Pinarbasi, H., Silig, Y., & Gurelic, M. (2005). Genetic polymorphisms of GSTs and their association with primary brain tumor incidence. Cancer Genetics and Cytogenetics, 156, 144–149.
Rebbeck, R. T. (1997). Molecular epidemiology of the human glutathione S-transferase genotypes GSTM1 and GSTT1 in cancer susceptibility. Cancer Epidemiology, Biomarkers and Prevention, 6, 733–743.
Lear, J., Heagerty, A., Smith, A., et al. (1996). Polymorphism in detoxifying enzymes and susceptibility to skin cancer. Photochemistry and Photobiology, 63, 424–428.
Helzlsouer, K. J., Selmin, O., Hung, H., et al. (1998). Association between glutathione S-transferase M1, P1 and T1 genetic polymorphisms and development of breast cancer. Journal of the National Cancer Institute, 90, 512–518.
Zhong, S., Wyllie, A. H., Barnes, D., et al. (1994). Relationship between the GSTM1 genetic polymorphism and susceptibility to bladder, breast and colon cancer. Carcinogenesis, 14, 1821–1824.
Trizna, Z., Clayman, G. L., Spitz, M. R., et al. (1995). Glutathione S-transferase genotypes as risk factors for head and neck cancer. American Journal of Surgery, 170, 499–501.
Pinarbasi, H., Silig, Y., Cetinkaya, O., et al. (2003). Strong association between the GSTM1-null genotype and lung cancer in a Turkish population. Cancer Genetics and Cytogenetics, 146, 125–129.
d’Errico, A., Tailor, J. A., Chen, X., et al. (1996). Genetic metabolic polymorphisms and the risk of cancer, a review of the literature. Biomarkers, 1, 149–173.
Ryberg, D., Skaug, V., Hewer, A., et al. (1997). Genotypes of glutathione S-transferase M1 and P1 and their significance for lung DNA adduct levers and cancer risk. Carcinogenesis, 18, 1285–1289.
Nelson, H. H., Wienche, J. K., Christiani, D. C., et al. (1995). Ethnic differences in the prevalence of the deleted genotype of glutathione S-transferase theta. Carcinogenesis, 16, 1243–1245.
Lee, E. J., Wong, J. Y., Yeoh, P. N., et al. (1995). Glutathione S-transferase theta (GSTT1) genetic polymorphism among Chinese, Malays and Indians in Singapore. Pharmacogenetics, 5, 332–334.
Kelsey, K. T., Wrensch, M., Zuo, Z. F., et al. (1997). A population based case-control study of the CYP2D6 and GSTT1 polymorphisms and malignant brain tumors. Pharmacogenetics, 7, 463–468.
Elexpuru, C. J., Buxton, N., Kandula, V., et al. (1995). Susceptibility to astrocytoma and meningioma: influence of allelism at glutathione S-transferase (GSTT1 and GSTM1) and cytochrome P450(CYP2D6) loci. Cancer Research, 55, 4237–4239.
Deakin, M., Elder, J., Hendrickse, D., et al. (1996). Glutathione S-transferase T1 genotypes and susceptibility to cancer: studies of interactions with GSTM1 in lung, oral, gastric and colorectal cancers. Carcinogenesis, 17, 881–884.
Watson, M. A., Stewart, R. K., Smith, G. B., et al. (1998). Human glutathione S-transferase P1 polymorphisms: relationship to lung tissue enzyme activity and population frequency distribution. Carcinogenesis, 19, 275–280.
Ye, Z., & Song, H. (2005). Glutathione S-transferase polymorphisms (GSTM1, GSTP1 and GSTT1) and the risk of acute leukaemia: a systematic review and meta-analysis. European Journal of Cancer, 41, 980–989.
Sbabrokb, M. G., Gbobadloo, M. S., Babram, Y., et al. (2004). GSTP1, GSTM1 and GSTT1 genetic polymorphisms in patients with cryptogenic liver cirrhosis. Journal of Gastrointestinal Surgery, 4, 423–427.
Beeghly, A., Katsaros, D., Chen, H., et al. (2006). Glutathione S-transferase polymorphisms and ovarian cancer treatment and survival. Gynecologic Oncology, 100, 330–337.
Sobti, R. C., Satinder, K., Pushpinder, K., et al. (2006). Interaction of passive smoking with GST (GSTM1, GSTT1 and GSTP1) genotypes in the risk of cervical cancer in India. Cancer Genetics and Cytogenetics, 166, 117–123.
Author information
Authors and Affiliations
Corresponding author
Rights and permissions
About this article
Cite this article
Ye, X., Jiang, Y., Wang, H. et al. Genetic polymorphisms of glutathione S-transferases are associated with ulcerative colitis in central China. Cell Biochem Biophys 60, 323–328 (2011). https://doi.org/10.1007/s12013-011-9154-z
Published:
Issue Date:
DOI: https://doi.org/10.1007/s12013-011-9154-z