Evaluation of oxidative stress and DNA damage in benign prostatic hyperplasia patients and comparison with controls

被引:30
作者
Ahmad M. [1 ]
Suhail N. [3 ]
Mansoor T. [1 ]
Banu N. [3 ,4 ]
Ahmad S. [2 ]
机构
[1] Department of General Surgery, J.N. Medical College, A.M.U., Aligarh
[2] Department of Pathology, J.N. Medical College, A.M.U., Aligarh
[3] Department of Biochemistry, Faculty of Life Sciences, A.M.U., Aligarh
[4] College of Medical Rehabilitation, Qassim University, Buraidah
关键词
Antioxidants; BPH; DNA damage; Lipid peroxidation; Oxidative stress;
D O I
10.1007/s12291-012-0229-4
中图分类号
学科分类号
摘要
In the present study, oxidative stress and lymphocytic DNA damage in both pre-op and post-op benign prostrate hyperplasia (BPH) patients with age >50 years was evaluated and compared with normal healthy subjects (controls- without any evidence of disease) of the same sex and age group. From December 2007 to November 2009, oxidative stress in 45 BPH patients were evaluated both before (pre-op patients) and after 7 days of surgery (post-op patients) in terms of measurements of plasma levels of (1) various anti-oxidative enzymes, (2) non-enzymatic antioxidants and (3) malondialdehyde which is a product of lipid peroxidation. The lymphocyte DNA damage was also evaluated by single cell alkaline gel electrophoresis in terms of tail length migration in these patients. These values were compared with their respective control subjects of similar sex and age group. The activities of antioxidant enzymes and the levels of antioxidant, reduced glutathione were found significantly decreased (p < 0.05) in serum samples of pre-operative group of BPH patients as compared to the controls. These altered parameters increased significantly (p < 0.05) and returned to their near normal control values, but not up to baseline values, in post operative patients i.e. after the cancer load was decreased by surgery. Lymphocytic DNA damage was found to be significantly increased in pre-op group as compared to controls and was reduced after surgery in post-op group. The present study therefore, shows significantly increased levels of oxidative stress and DNA damage in BPH patients which were reduced after removal of tumour load. Thus oxidative damage plays an important role in prostate tumourogenesis and timely management of oxidative stress can be of importance in preventing the occurrence of BPH. © 2012 Association of Clinical Biochemists of India.
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页码:385 / 388
页数:3
相关论文
共 19 条
[1]  
Nelson W.G., De Marzo A.M., Isaacs W.B., Prostate cancer, N Engl J Med, 349, pp. 366-381, (2003)
[2]  
Malins D.C., Johnson P.M., Barker E.A., Polissar N.L., Wheeler T.M., Anderson K.M., Cancer-related changes in prostate DNA as men age and early identification of metastasis in primary prostate tumors, Proc Natl Acad Sci USA, 100, pp. 5401-5406, (2003)
[3]  
Ripple M.O., Henry W.F., Rago R.P., Et al., Prooxidant-antioxidant shift induced by androgen treatment of human prostate carcinoma cells, J Natl Cancer Inst, 89, 1, pp. 40-48, (1997)
[4]  
Buege J.A., Aust S.D., Microsomal lipid peroxidation, Methods Enzymol, 52, pp. 302-310, (1978)
[5]  
Marklund S.L., Extracellular superoxide dismutase in human tissues and human cell lines, J Clin Invest, 74, pp. 1398-1403, (1984)
[6]  
Claiborne A., Catalase activity, CRC Handbook of Methods for Oxygen Radical Research, pp. 283-284, (1985)
[7]  
Carlberg I., Mannervik B., Purification and characterization of the flavoenzyme glutathione reductase from rat liver, J Biol Chem, 250, pp. 5475-5480, (1975)
[8]  
Habig W.H., Pabst M.J., Jacoby W.H., Glutathione-S-transferases: The first step in mercapturic acid formation, J Biol Chem, 249, pp. 7130-7139, (1974)
[9]  
Jollow D.J., Mitchell J.R., Zampaglione N., Gillete J.R., Bromobenzene induced liver necrosis: Protective role of glutathione and evidence for 3,4-bromobenzene oxide as the hepatotoxic intermediate, Pharmacology, 11, pp. 151-169, (1974)
[10]  
Singh N.P., McCoy M.T., Tice R.R., Schneider E.L., A simple technique for quantitation of low levels of DNA damage in individual cells, Exp Cell Res, 175, pp. 184-191, (1988)