Objective: Prostate cancer is the leading cause of cancer-related deaths. Oxidative DNA damage may contribute to the prostate cancer. The paraoxonase (PON1) is an endogenous antioxidant in the human body. The aim of our study was to determine whether lipid parameters, total oxidant capacity (TOC), total antioxidant capacity (TAC), oxidative stress index (OSİ), serum paraoxonase (PON1) and arylesterase (ARE) levels and phenotypes distribution alter new diagnosis in patients with prostate cancer and to compare the values with those of healthy controls. Methods: The study was performed prospective which consist of the prostate cancer group (PC) and healthy control group. Serum PON1, ARE activities, and other parameters were measured in 40 subjects in both groups. The PON1 phenotypes were defined according to the ratio of serum PON1/ARE activity. In statistical evaluation of data was performed by Student t test and Pearson’s correlation analysis. Results: TKOL and LDL-K levels were found to be lower in the patients compared to controls (p=0,044; p=0,026). OSI levels in patients was higher than the controls (p=0,029). PON1 and ARE activities were found to be lower in patients compared to the controls (p=0,040; p=0,027). PON1 enzyme activity was determined as three different phenotypes in both groups. In PC group, significant deviation of PON1 phenotype frequencies from Hardy–Weinberg equilibrium was found. Conclusion: The results of our study suggest that oxidative stress, through lipid peroxidation may play an important role for the development of prostate cancer and that PON1, and PON1 phenotyping may be predictive for prostate cancer
Amaç: Prostat kanseri, kansere bağlı ölümlerin önemli nedenlerinden biridir. Oksidatif DNA hasarının prostat kanseri gelişmesine katkıda bulunabileceği belirtilmektedir. antioksidanlardan biridir. Çalışmamızda yeni tanı almış prostat kanserli hastalarda (PON)
Primary Language | Turkish |
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Journal Section | Articles |
Authors | |
Publication Date | August 1, 2015 |
Published in Issue | Year 2015 Volume: 7 Issue: 2 |