Dergiler / KONURALP TIP DERGİSİ / 2015 / Cilt: 7 - Sayı: 2

Prostat Kanserli Hastalarda Oksidatif Stres ve Paraksonaz Aktivite Azalması

-

Sayfa
113–117
DOI
—
🏛️Bu makalenin bibliyografik verileri ve tam metin bağlantısı DergiPark üzerinden sağlanmıştır.
DergiPark Kaydı ↗
✨

Yapay Zeka Hızlı Bakış & Çıkarımlar

AI Insight
⚡ TL;DR(1 Cümlede Hızlı Çıkarım)

Çalışmamızda yeni tanı almış prostat kanserli hastalarda (PON)

📌 3 Maddede Bu Makale

🎯
Amaç & Hipotez:Amaç: Prostat kanseri, kansere bağlı ölümlerin önemli nedenlerinden biridir.
📊
Temel Bulgular & Veri:Oksidatif DNA hasarının prostat kanseri gelişmesine katkıda bulunabileceği belirtilmektedir. antioksidanlardan biridir.
💡
Sonuç & Katkı:Çalışmamızda yeni tanı almış prostat kanserli hastalarda (PON)
🔬Tür:Araştırma Makalesi
📍Kapsam:Genişletilmiş Akademik Örneklem
⚙️Değişkenler:Oksidatif Stres · Lipid Peroksidasyonu · Paraoksonaz

Özet

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)

Abstract

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

🔖

Bu Makaleye Atıf Yap

ORHAN, N., ÖZCAN, M. E., MEMİŞOĞULLARI, R., UÇGUN, T., KAYIKÇI, M. A., DEMİRİN, H. (2015). Prostat Kanserli Hastalarda Oksidatif Stres ve Paraksonaz Aktivite Azalması. KONURALP TIP DERGİSİ, Cilt: 7 - Sayı: 2, 113–117. https://ajindex.com/articles/205256

📄 Tam Metin PDF Okuyucu

📄

PDF görüntüleyici hazırlanıyor...

Kaynakça (16)

  1. Engin A, Altan N. Effects of obstructive jaundice on the antioxidative capacity of human red blood cells. Hematologia. 2000;30(2):91-6.
  2. Yardım-Akaydın S, Sepici A, Özkan Y, Torun M, Şimşek B, Sepici V. Oxidation of Uric Acid in Rheumatoid Arthritis: Is Allontoin a Marker of Oxidative Stress? Free Radic Res. 2004;38(6):623-8. Babior BM. Phagocytes and oxidative stress. Am J Med. 2000;109(1):33-44.
  3. Jackson AL, Loeb LA. The contribution of endogenous sources of DNA damage to the multiple mutations in cancer. Mutat Res 2001; 477(1-2):7-21.
  4. Behrend L, Henderson G, Zwacka RM. Reactive oxygen species in oncogenic transformation. Biochem Soc Trans. 2003; 31(Pt 6):1441-4.
  5. Cobanoglu U, Demir H, Duran M. Erytrocyte catalase and carbonic anhydrase activities in lung cancer. Asian Pac J Cancer Prev. 2010; 11(5):1377-82.
  6. Blatter MC, James RW, Messmer S, Barja F, Pometta D. Identification of a distinct human high-density lipoprotein subspecies defined by a lipoprotein-associated protein, K-45. Identity of K-45 with paraoxonase. Eur J Biochem. 1993; 211(3):871-9.
  7. Mackness MI, Arrol S, Durrington PN. Paraoxonase prevents accumulation of lipoperoxides in low-density lipoprotein. FEBS Lett. 1991; 286:152-4.
  8. Greenlee RT, Murray T, Bolden S, Wingo PA. Cancer statistics, 2000. CA Cancer J Clin. 2000; 50(1):7–33.
  9. Echerson HW, Wyte CM, La Du BN. The human serum paraoxonase/arylesterase polymorphizm. Am J Hum Genet. 1983; 35(6):1126-38.
  10. Srivastava D, Mittal RD. Free radical injury and antioxidant status in patients with benign prostate hyperplasia and prostate cancer. Indian Journal of Clinical Biochemistry. 2005; 20(2):162-5.
  11. Elkiran TE, Mar N, Aygen B, Gursu F, Karaoglu A, Koca S. Serum paraoxonase and arylesterase activities in patients with lung cancer in a Turkish population. BMC Cancer. 2007; 16:7-48.
  12. Akcay MN, Polat MF, Yilmaz I, Akcay G. Serum paraoxonase levels in pancreatic cancer. Hepatogastroenterology. 2003; 50(2):225–7.
  13. Akcay MN, Polat MF, Yilmaz I, Akcay G. Serum paraoxonase levels in gastric cancer. Hepatogastroenterology. 2003; 50(2):273–5.
  14. Başkol M, Başkol G, Koçer D. Mide kanserli hastalarda oksidan ve antioksidan parametreler ve birbiriyle ilişkileri. Türk Klinik Biyokimya Derg. 2007; 5(3):83-9.
  15. Kumon Y, Nakauchi Y, Suehiro T. Proinflammatory cytokines but not acute phase serum amyloid A or C- reactive protein, downregulate paraoxonase 1 (PON1) expression by HepG2. Amyloid. 2002; 9(3):160-4.
  16. Macri A, Versaci A, Loddo S. Serum levels of interleukin 1beta, interl