Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Lower Thiol, Glutathione, and Glutathione Peroxidase Levels in Prostate Cancer: A Meta-Analysis Study

Version 1 : Received: 1 June 2020 / Approved: 2 June 2020 / Online: 2 June 2020 (09:27:21 CEST)

How to cite: Sajjaboontawee, N.; Supasitthumrong, T.; Tunvirachaisakul, C.; Nantachai, K.; Snabboon, T.; Reiche, E.M.V.; Simão, A.N.C.; Maes, M. Lower Thiol, Glutathione, and Glutathione Peroxidase Levels in Prostate Cancer: A Meta-Analysis Study. Preprints 2020, 2020060003. https://doi.org/10.20944/preprints202006.0003.v1 Sajjaboontawee, N.; Supasitthumrong, T.; Tunvirachaisakul, C.; Nantachai, K.; Snabboon, T.; Reiche, E.M.V.; Simão, A.N.C.; Maes, M. Lower Thiol, Glutathione, and Glutathione Peroxidase Levels in Prostate Cancer: A Meta-Analysis Study. Preprints 2020, 2020060003. https://doi.org/10.20944/preprints202006.0003.v1

Abstract

Introduction: Lowered thiol or sulfhydryl (-SH) groups and glutathione (GSH) metabolism may be associated with prostate cancer (PCa) and benign prostatic hyperplasia (BPH). The main objectives of this study were to systematically review and meta-analyze the evidence on the associations among -SH groups, GSH, GSH peroxidase (GPx), GSH reductase (GR) and GSH transferase (GST) and PCa/BPH. Methods: Four electronic databases were searched for studies that reported -SH and GSH variables in PCa/BPH and healthy controls (HC) and the data were meta-analyzed by calculating Hedges’s g with 95% confidence intervals. Results: Twenty studies were included in this meta-analysis including 800 PCa and 791 BPH patients and 592 HC. Total -SH (g=-1.750, -2.341/-1.159), GPx (g=-0.789, -1.234/-0.344), GSH (g=-2.219, -4.132/-0.305), and the combination of -SH, GPx, and GSH (g=-1.271, -1.271/-0.800) were significantly lower in PCa patients than in HC. -SH (g=-1.752, -3.123/-0.381) and the combination of -SH, GPx, and GSH (g=-0.813, -1.298/-0.327) were significantly lower in BPH patients than in HC. GPx was significantly lower in PCa than in BPH patients (g=-0.455, -0.896/-0.014). Heterogeneity levels were very high, but Egger’s test showed that none of the biomarkers showed significant publication bias. Conclusion: Thiol/GPx antioxidant defenses are significantly attenuated in patients with PCa while patients with BPH occupy an intermediate risk group position between PCa patients and HC. Those results suggest that reduced thiol-related antioxidant mechanisms play a crucial role in prostatic disorders, especially in PCa. Future research should examine whether thiols/GPx antioxidants are associated with the onset of PCa/BHP.

Keywords

antioxidants; oxidative stress; prostate cancer; benign prostatic hyperplasia; biomarkers; pathways

Subject

Medicine and Pharmacology, Urology and Nephrology

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