2010, Number 3
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Rev Mex Urol 2010; 70 (3)
Regulation of antioxidant enzymes as prostate tumor markers
Estrada-Carrasco CE, Flores-Terrazas JE, Floriano-Sánchez E, Castro-Marín M, López-Silvestre JL, Campos-Salcedo JG, Zapata-Villalba MA, Mendoza-Álvarez LA, Cárdenas-Rodríguez N
Language: Spanish
References: 13
Page: 157-163
PDF size: 663.48 Kb.
ABSTRACT
Background: Prostate cancer has recently been reported to be in third place worldwide; in Mexico it is the principal cause of death by cancer in men after lung cancer. Oxidative stress has been observed to play a role in cancer etiology. Catalase is a peroxisome-specific antioxidant enzyme in mammals and is an important inflammation and oxidative stress regulator. Superoxide dismutase (SOD1) is an antioxidant enzyme that facilitates dismutation of oxygen radicals to hydrogen peroxide and also catalyzes pro-oxidant reactions. In the present study, catalase and SOD-1 antioxidant enzyme expression was determined in prostate cancer and benign prostatic hyperplasia.
Methods: A total of 40 samples of benign prostatic hyperplasia tissue and 40 samples of prostate cancer tissue were obtained. Conditions were standardized to immunohistochemically detect the presence of catalase and SOD-1 in the tissues.
Results: The percentage of the area that was immunoreactive to catalase and to SOD-1 was greater in prostate cancer tissue than in benign prostatic hyperplasia tissue.
Conclusions: Densitometric expression and percentage of the area marked with catalase and SOD-1 antioxidant enzymes per field was higher in prostate cancer tissue than in benign prostatic cancer tissue.
REFERENCES
Dirección General de Epidemiología; SSA, México. Compendio de Cáncer 1998-2002.
Jemal A, Murray T, Ward E. Cancer statistics 2005. CA Cancer J Clin. 2005;55(1):10-30.Rubin MA, De Marzo AM. Molecular genetics of prostate cancer. Mod Pathol 2004;17(3):380-388.
Parkin DM, Whelan SL, Ferlay J, Teppo L, Thomas DB, editors. Cancer Incidence in Five Continents Vol. VIII. IARC Scientific Publications No. 155. Lyon, France: IARC 2002.
Nilsson S, Norlén BJ, Widmark A. A systematic overview of radiation therapy effects in prostate cancer. Acta Oncol 2004;43(4):316-318.
Nelson PS. In. Prostate, Cancer, Biology, Genetics, and the New Therapeutics. Eds, Chung, LWKIsaacs, WB Simons, JW; Humana Press Inc. Totowa NJ. 2001, 175-189.
Coussens LM, Werb Z. Inflammation and cancer. Nature 2002;420(6917):860-867.
Adam BL, Qu Y, Davis JW. Serum protein fingerprinting coupled with a pattern-matching algorithm distinguishes prostate cancer from benign prostate hyperplasia and healthy men. Cancer Res 2002;62(13):3609-3614.
Noor R, Mittal S, Iqbal J. Superoxide dismutase-applications and relevance to human diseases. Med Sci Monit 2002;8(9):RA210-215.
Baker AM, Oberley LW, Cohen MB. Expression of antioxidant enzymes in prostatic adenocarcinoma. Prostate 1997;32(4):229-233.
Pryor WA. Forum on oxidative stress status (OSS) and its measurement. Free Radic Biol Med 2000;29(5):387.
Morel Y, Barouki R. Repression of gene expression by oxidative stress. Biochem J 1999;342 Pt 3:481-496.
Ripple O, William F, Randall P,Wilding G. Prooxidant–antioxidant shift induced by androgen treatment of human prostate carcinoma cells. J Natl Cancer Inst 1997;89(1):40-48.
Hamilton ML, Van Remmen H. Does oxidative damage to DNA increase with age? Proc Natl Acad Sci U S A 2001;98(18):10469-10474.