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Free radical injury and antioxidant status in patients with benign prostate hyperplasia and prostate cancer

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Abstract

Reactive oxygen species and other free radicals are known to be the mediators of phenotypic and genotypic changes that lead from mutation to neoplasia. There are some primary antioxidants such as glutathione peroxidase (GPx), glutathione S-transferases (GSTs) and reduced glutathione, which protect against callular and molecular damage caused by the reactive oxygen metabolites (ROMs). The present study was conducted to determine the level of malondialdehyde (MDA), as an index of lipid peroxidation, along with the GPx, GSTs activities and level of reduced glutathione in 45 prostate cancer (PC) patients, 55 benign prostate hyperplasia (BPH) patients as compared to the controls. Significant higher levels of MDA and GSTs activities in the serum, (P<0.005) and significant lower levels of reduced GSH concentration and GPx activity in blood haemolysates (P<0.05) of PC and BPH patients were observed as compared to the controls. The relatively higher GSTs activity and low level of reduced GSH may be due to the response of increased reactive oxygen metabolites production in the blood. The higher MDA and lower GPx activities may be inadequate to detoxify high levels of H2O2 into H2O leading to the formation of the*OH radical followed by MDA. This result hypothesizes that oxidant-antioxidant imbalance may be one of the major factor responsible for the development of prostate cancer and benign prostate hyperplasia.

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Authors and Affiliations

  1. Department of Urology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Raebareli Road, 226014, Lucknow, India

    D. S. L. Srivastava & R. D. Mittal (Additional Professor)

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  1. D. S. L. Srivastava
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  2. R. D. Mittal
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Correspondence to R. D. Mittal.

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Srivastava, D.S.L., Mittal, R.D. Free radical injury and antioxidant status in patients with benign prostate hyperplasia and prostate cancer. Indian J Clin Biochem 20, 162–165 (2005). https://doi.org/10.1007/BF02867419

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