ACTIVITY OF ENZYMES OF THE PRO-/ANTIOXIDANT SYSTEM IN BENIGN PROSTATIC HYPERPLASIA
DOI: http://dx.doi.org/10.30970/sbi.2003.902
Abstract
Background. Benign prostatic hyperplasia (BPH), which is mostly prevalent in older men, is associated with compression of the prostatic urethra and manifests as lower urinary tract symptoms. Its pathological characteristics include abnormal proliferation of stromal and glandular epithelial cells, leading to prostate enlargement. Current data highlight additional factors in the pathogenesis of this disease, notably oxidative stress and chronic inflammation.
Materials and Methods. Prostate tissue was obtained from 35 patients aged 58–72 years via transurethral resection. Prostate tissue from three patient groups was utilized. Group 1 consisted of patients with BPH (n = 7) weighing up to 40 grams (control group); Group 2 included patients with BPH (n = 14) weighing 45–98 grams; Group 3 comprised patients with benign prostatic hyperplasia and chronic inflammation (adenoprostatitis) weighing 45–98 grams (n = 14). The levels of malondialdehyde and reduced glutathione, as well as the activities of glutathione peroxidase and glutathione reductase, were determined in the tissues.
Results. In large-scale prostate hyperplasia and prostate hyperplasia associated with prostatitis, lipid peroxidation processes escalate in prostate cells, as indicated by an increase in malondialdehyde concentration. The elevation in lipid peroxidation levels is accompanied by a decrease in the activity of antioxidant defense enzymes glutathione peroxidase and glutathione reductase, alongside a reduction in the concentration of reduced glutathione. The balance within the pro-/antioxidant system is more significantly disrupted in cases of prostate hyperplasia associated with prostatitis.
Conclusion. In large-scale prostate hyperplasia and hyperplasia associated with histologically confirmed prostatitis, lipid peroxidation processes intensify within the cells, which is confirmed by rising levels of malondialdehyde. The increase in lipid peroxidation is accompanied by a decline in glutathione peroxidase and glutathione reductase activities, as well as a decrease in the concentration of reduced glutathione. In prostate hyperplasia accompanied by adenoprostatitis, the balance in the pro-/antioxidant system is disrupted to a greater extent.
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| Anderson, M. E. (1985). Determination of glutathione and glutathione disulfide in biological samples. In R. A. Greenwald (Ed.), Handbook of methods for oxygen radical research (Methods in enzymology, Vol. 113, pp. 548-555). Elsevier. doi:10.1016/s0076-6879(85)13073-9 Crossref ● PubMed ● Google Scholar | ||||
| ||||
| Bostanci, Y., Kazzazi, A., Momtahen, S., Laze, J., & Djavan, B. (2013). Correlation between benign prostatic hyperplasia and inflammation. Current Opinion in Urology, 23(1), 5-10. doi:10.1097/mou.0b013e32835abd4a Crossref ● PubMed ● Google Scholar | ||||
| ||||
| Carson, C., III, & Rittmaster, R. (2003). The role of dihydrotestosterone in benign prostatic hyperplasia. Urology, 61(4), 2-7. doi:10.1016/s0090-4295(03)00045-1 Crossref ● PubMed ● Google Scholar | ||||
| ||||
| Chughtai, B., Lee, R., Te, A., & Kaplan, S. (2011). Role of inflammation in benign prostatic hyperplasia. Reviews in Urology, 13(3), 147-150. PubMed ● PMC ● Google Scholar | ||||
| ||||
| Forrester, S. J., Kikuchi, D. S., Hernandes, M. S., Xu, Q., & Griendling, K. K. (2018). Reactive oxygen species in metabolic and inflammatory signaling. Circulation Research, 122(6), 877-902. doi:10.1161/circresaha.117.311401 Crossref ● PubMed ● PMC ● Google Scholar | ||||
| ||||
| Grutman, A. J., Su, Z. T., & Herati, A. S. (2025). Testosterone effects on the prostate: focusing on benign prostatic hyperplasia. In B. R. Zirkin, I. Huhtaniemi, D. J. Lamb, & V. Papadopoulos (Eds.), Leydig cells: formation, regulation and function in health and disease (pp. 785-801). Springer. doi:10.1007/978-3-031-96376-6_31 Crossref ● Google Scholar | ||||
| ||||
| Inamura, S., & Terada, N. (2024). Chronic inflammation in benign prostatic hyperplasia: pathophysiology and treatment options. International Journal of Urology, 31(10), 968-974. doi:10.1111/iju.15518 Crossref ● PubMed ● PMC ● Google Scholar | ||||
| ||||
| Kaltsas, A., Giannakas, T., Stavropoulos, M., Kratiras, Z., & Chrisofos, M. (2025). Oxidative stress in benign prostatic hyperplasia: mechanisms, clinical relevance and therapeutic perspectives. Diseases, 13(2), 53. doi:10.3390/diseases13020053 Crossref ● PubMed ● PMC ● Google Scholar | ||||
| ||||
| Kushynska, M. E., Onufrovych, O. K., Vorobets, D. Z., Besedina, A. S., Galyk, G. V., Pershyn, O. I., Fafula, R. V., & Vorobets, Z. D. (2025). Kinetic properties of glutathione-S-transferase in prostate gland biopsies of patients with benign prostatic hyperplasia and chronic prostatitis. Regulatory Mechanisms in Biosystems, 16(4), e25164. doi:10.15421/0225164 Crossref ● Google Scholar | ||||
| ||||
| Lambeth, J. D. (2007). Nox enzymes, ROS, and chronic disease: an example of antagonistic pleiotropy. Free Radical Biology and Medicine, 43(3), 332-347. doi:10.1016/j.freeradbiomed.2007.03.027 Crossref ● PubMed ● PMC ● Google Scholar | ||||
| ||||
| Lee, K. L., & Peehl, D. M. (2004). Molecular and cellular pathogenesis of benign prostatic hyperplasia. Journal of Urology, 172(5), 1784-1791. doi:10.1097/01.ju.0000133655.71782.14 Crossref ● PubMed ● Google Scholar | ||||
| ||||
| Liou, G.-Y., C'lay-Pettis, R., & Kavuri, S. (2024). Involvement of reactive oxygen species in prostate cancer and its disparity in African descendants. International Journal of Molecular Sciences, 25(12), 6665. doi:10.3390/ijms25126665 Crossref ● PubMed ● PMC ● Google Scholar | ||||
| ||||
| Nabil, H., Moemen, L. A., & Abu Elela, M. H. (2008). Studying the levels of malondialdehyde and antioxidant parameters in normal and abnormal human seminal plasma. Australian Journal of Basic and Applied Sciences, 2(3), 773-778. Google Scholar | ||||
| ||||
| Pisoschi, A. M., Pop, A., Iordache, F., Stanca, L., Predoi, G., & Serban, A. I. (2021). Oxidative stress mitigation by antioxidants - an overview on their chemistry and influences on health status. European Journal of Medicinal Chemistry, 209, 112891. doi:10.1016/j.ejmech.2020.112891 Crossref ● PubMed ● Google Scholar | ||||
| ||||
| Raijmakers, M. T., Roelofs, H. M., Steegers, E. A., Steegers-Theunissen, R. P. M., Mulder, T. P., Knapen, M. F., Wong, W. Y., & Peters, W. H. (2003). Glutathione and glutathione S-transferases A1-1 and P1-1 in seminal plasma may play a role in protecting against oxidative damage to spermatozoa. Fertility and Sterility, 79(1), 169-172. doi:10.1016/s0015-0282(02)04404-7 Crossref ● PubMed ● Google Scholar | ||||
| ||||
| Sajjaboontawee, N., Supasitthumrong, T., Tunvirachaisakul, C., Nantachai, K., Snabboon, T., Reiche, E. M. V., Simão, A. N. C., & Maes, M. (2020). Lower thiol, glutathione, and glutathione peroxidase levels in prostate cancer: a meta-analysis study. Aging Male, 23(5), 1533-1544. doi:10.1080/13685538.2020.1858048 Crossref ● PubMed ● Google Scholar | ||||
| ||||
| Shukla, S., Srivastava, J. K., Shankar, E., Kanwal, R., Nawab, A., Sharma, H., Bhaskaran, N., Ponsky, L. E., Fu, P., MacLennan, G. T., & Gupta, S. (2020). Oxidative stress and antioxidant status in high-risk prostate cancer subjects. Diagnostics, 10(3), 126. doi:10.3390/diagnostics10030126 Crossref ● PubMed ● PMC ● Google Scholar | ||||
| ||||
| Tramer, F., Caponecchia, L., Sgrò, P., Martinelli, M., Sandri, G., Panfili, E., Lenzi, A., & Gandini, L. (2004). Native specific activity of glutathione peroxidase (GPx-1), phospholipid hydroperoxide glutathione peroxidase (PHGPx) and glutathione reductase (GR) does not differ between normo- and hypomotile human sperm samples. International Journal of Andrology, 27(2), 88-93. doi:10.1046/j.1365-2605.2003.00452.x Crossref ● PubMed ● Google Scholar | ||||
| ||||
| Valgimigli, L. (2023). Lipid peroxidation and antioxidant protection. Biomolecules, 13(9), 1291. doi:10.3390/biom13091291 Crossref ● PubMed ● PMC ● Google Scholar | ||||
| ||||
| Wang, G., Lv, C., Liu, Z., Huang, M., Zhang, Y., Chen, J., Hu, J., Jin, Y., & Bai, Z. (2025). Gland- and cell-level heterogeneity in the prostate: a narrative review of related diseases. Current Urology, 19(4), 241-246. doi:10.1097/cu9.0000000000000269 Crossref ● PubMed ● PMC ● Google Scholar | ||||
| ||||
| Weldy, C. S., Luttrell, I. P., White, C. C., Morgan-Stevenson, V., Bammler, T. K., Beyer, R. P., Afsharinejad, Z., Kim, F., Chitaley, K., & Kavanagh, T. J. (2012). Glutathione (GSH) and the GSH synthesis gene Gclm modulate vascular reactivity in mice. Free Radical Biology and Medicine, 53(6), 1264-1278. doi:10.1016/j.freeradbiomed.2012.07.006 Crossref ● PubMed ● PMC ● Google Scholar | ||||
| ||||
| Ye, Z., Wang, J., Xiao, Y., Luo, J., Xu, L., & Chen, Z. (2024). Global burden of benign prostatic hyperplasia in males aged 60-90 years from 1990 to 2019: results from the global burden of disease study 2019. BMC Urology, 24(1), 193. doi:10.1186/s12894-024-01582-w Crossref ● PubMed ● PMC ● Google Scholar | ||||
| ||||
| Zabaiou, N., Mabed, D., Lobaccaro, J. M., & Lahouel, M. (2016). Oxidative stress in benign prostate hyperplasia. Andrologia, 48(1), 69-73. doi:10.1111/and.12420 Crossref ● PubMed ● Google Scholar | ||||
| ||||
| Zhang, Y., Hu, X., & Zou, L.-Q. (2024). Flavonoids as therapeutic agents for epilepsy: unveiling anti-inflammatory and antioxidant pathways for novel treatments. Frontiers in Pharmacology, 15, 1457284. doi:10.3389/fphar.2024.1457284 Crossref ● PubMed ● PMC ● Google Scholar | ||||
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