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      Oxidative stress adaptation in aggressive prostate cancer may be counteracted by the reduction of glutathione reductase

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          Highlights

          ► Oxidative stress was evaluated on a cell line model of prostate cancer progression. ► Metastatic cell lines show the highest ROS, total antioxidant status and resistance to H 2O 2. ► Metastatic cell lines show the highest levels of GSH and Gl-Red activity. ► Decrease in GSH levels and Gl-Red activity induced a decrease in H 2O 2 resistance. ► Gl-Red activity reduction may be a new therapeutic approach in prostate cancer.

          Abstract

          Oxidative stress has been associated with prostate cancer development and progression due to an increase of reactive oxygen species (ROS). However, the mechanisms whereby ROS and the antioxidant system participate in cancer progression remain unclear.

          In order to clarify the influence of oxidative stress in prostate cancer progression, we performed this study in two human prostate cancer cell lines, PC3 and HPV10 (from metastasis and from localized cancer, respectively) and RWPE1 cells derived from normal prostate epithelium. Cells were treated with hydrogen peroxide (H 2O 2) and PC3 cells were also treated with diethyl maleate (DEM). The effect on cell growth, viability, mitochondria membrane potential and oxidative stress was analysed. Oxidative stress was evaluated based on ROS production, oxidative lesion of lipids (MDA) and on determination of antioxidants, including enzyme activity of glutathione peroxidase (Gl-Px), glutathione reductase (Gl-Red) and on the quantification of glutathione (GSH), glutathione-s-transferase (GST) and total antioxidant status (TAS).

          PC3 shows higher ROS production but also the highest GSH levels and Gl-Red activity, possibly contributing to oxidative stress resistance. This is also associated with higher mitochondrial membrane potential, TAS and lower lipid peroxidation. On the other hand, we identified Gl-Red activity reduction as a new strategy in overcoming oxidative stress resistance, by inducing H 2O 2 cytotoxicity. Therefore these results suggest Gl-Red activity reduction as a new potential therapeutic approach, in prostate cancer.

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          Most cited references46

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          Cancer Statistics, 2008

          A. Jemal, R. Siegel, E. Ward … (2008)
          Each year, the American Cancer Society estimates the number of new cancer cases and deaths expected in the United States in the current year and compiles the most recent data on cancer incidence, mortality, and survival based on incidence data from the National Cancer Institute, Centers for Disease Control and Prevention, and the North American Association of Central Cancer Registries and mortality data from the National Center for Health Statistics. Incidence and death rates are age-standardized to the 2000 US standard million population. A total of 1,437,180 new cancer cases and 565,650 deaths from cancer are projected to occur in the United States in 2008. Notable trends in cancer incidence and mortality include stabilization of incidence rates for all cancer sites combined in men from 1995 through 2004 and in women from 1999 through 2004 and a continued decrease in the cancer death rate since 1990 in men and since 1991 in women. Overall cancer death rates in 2004 compared with 1990 in men and 1991 in women decreased by 18.4% and 10.5%, respectively, resulting in the avoidance of over a half million deaths from cancer during this time interval. This report also examines cancer incidence, mortality, and survival by site, sex, race/ethnicity, education, geographic area, and calendar year, as well as the proportionate contribution of selected sites to the overall trends. Although much progress has been made in reducing mortality rates, stabilizing incidence rates, and improving survival, cancer still accounts for more deaths than heart disease in persons under age 85 years. Further progress can be accelerated by supporting new discoveries and by applying existing cancer control knowledge across all segments of the population.
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            Inflammation in prostate carcinogenesis.

            Angelo M. De Marzo, Elizabeth A. Platz, Siobhan Sutcliffe … (2007)
            About 20% of all human cancers are caused by chronic infection or chronic inflammatory states. Recently, a new hypothesis has been proposed for prostate carcinogenesis. It proposes that exposure to environmental factors such as infectious agents and dietary carcinogens, and hormonal imbalances lead to injury of the prostate and to the development of chronic inflammation and regenerative 'risk factor' lesions, referred to as proliferative inflammatory atrophy (PIA). By developing new experimental animal models coupled with classical epidemiological studies, genetic epidemiological studies and molecular pathological approaches, we should be able to determine whether prostate cancer is driven by inflammation, and if so, to develop new strategies to prevent the disease.
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              Malondialdehyde determination as index of lipid peroxidation.

              H. Draper, M Hadley (1990)
              Article 0 comments Cited 393 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Mariana Freitas
                Inês Baldeiras
                Teresa Proença
                Vera Alves
                Anabela Mota-Pinto
                Ana Sarmento-Ribeiro
                Journal
                Journal ID (nlm-ta): FEBS Open Bio
                Journal ID (iso-abbrev): FEBS Open Bio
                Title: FEBS Open Bio
                Publisher: Elsevier
                ISSN (Electronic): 2211-5463
                Publication date PMC-release: 30 May 2012
                Publication date (Electronic): 30 May 2012
                Publication date Collection: 2012
                Volume: 2
                Pages: 119-128
                Affiliations
                [a ]General Pathology Laboratory, Faculty of Medicine, University of Coimbra, Rua Larga, 3004-504 Coimbra, Portugal
                [b ]CIMAGO – Centre of Investigation in Environment, Genetics and Oncobiology, Faculty of Medicine, University of Coimbra, Apartado, 9015 3001-301 Coimbra, Portugal
                [c ]CNC – Centre of Neurosciences and Cell Biology, Department of Zoology, University of Coimbra, 3004-517 Coimbra, Portugal
                [d ]Laboratory of Neurochemistry, Neurology Department, Hospital of the University of Coimbra, Praceta Prof Mota Pinto, 3000-075 Coimbra, Portugal
                [e ]Immunology Laboratory, Faculty of Medicine, University of Coimbra, Rua Larga, 3004-504 Coimbra, Portugal
                [f ]Applied Molecular Biology/Biochemistry Laboratory and Haematology, Faculty of Medicine, University of Coimbra, Subunidade I de Ensino, Pólo III, 3000-354 Coimbra, Portugal
                Author notes
                [* ]Corresponding author at: General Pathology Laboratory, Faculty of Medicine, University of Coimbra, Rua Larga, 3004-504 Coimbra, Portugal. Fax: 351 239 822 547. freitas.mariana@ 123456gmail.com
                [1]

                Fax: +351 239 721 478.

                [2]

                Fax: +351 239 823 907.

                [3]

                Fax: +351 239 820 242.

                [4]

                Fax: +351 239 480 048.

                Article
                Publisher ID: FOB23
                DOI: 10.1016/j.fob.2012.05.001
                PMC ID: 3642126
                PubMed ID: 23650590
                SO-VID: 0d183a38-a204-4f98-95b8-12dc49e1f38d
                Copyright © © 2012 Published by Elsevier B.V. on behalf of Federation of European Biochemical Societies.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-No Derivative Works License, which permits non- commercial use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date received : 16 March 2012
                Date revision received : 10 May 2012
                Date accepted : 11 May 2012
                Categories
                Subject: Article

                Keywords: prostate cancer,oxidative stress (os),reactive oxygen species (ros),glutathione (gsh),glutathione reductase (gl-red),cell line
                Data availability:
                Keywords: prostate cancer, oxidative stress (os), reactive oxygen species (ros), glutathione (gsh), glutathione reductase (gl-red), cell line

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