BibTex RIS Kaynak Göster

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Yıl 2015, Cilt: 7 Sayı: 2, 113 - 117, 01.08.2015
https://doi.org/10.18521/ktd.63203

Öz

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

Kaynakça

  • Engin A, Altan N. Effects of obstructive jaundice on the antioxidative capacity of human red blood cells. Hematologia. 2000;30(2):91-6.
  • 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.
  • 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.
  • Behrend L, Henderson G, Zwacka RM. Reactive oxygen species in oncogenic transformation. Biochem Soc Trans. 2003; 31(Pt 6):1441-4.
  • 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.
  • 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.
  • Mackness MI, Arrol S, Durrington PN. Paraoxonase prevents accumulation of lipoperoxides in low-density lipoprotein. FEBS Lett. 1991; 286:152-4.
  • Greenlee RT, Murray T, Bolden S, Wingo PA. Cancer statistics, 2000. CA Cancer J Clin. 2000; 50(1):7–33.
  • Echerson HW, Wyte CM, La Du BN. The human serum paraoxonase/arylesterase polymorphizm. Am J Hum Genet. 1983; 35(6):1126-38.
  • 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.
  • 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.
  • Akcay MN, Polat MF, Yilmaz I, Akcay G. Serum paraoxonase levels in pancreatic cancer. Hepatogastroenterology. 2003; 50(2):225–7.
  • Akcay MN, Polat MF, Yilmaz I, Akcay G. Serum paraoxonase levels in gastric cancer. Hepatogastroenterology. 2003; 50(2):273–5.
  • 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.
  • 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.
  • Macri A, Versaci A, Loddo S. Serum levels of interleukin 1beta, interleukin 8 and tumour necrosis factor alpha as markers of gastric cancer. Biomarkers. 2006; 11(2):184-93.
  • Van Lenten BJ, Wagner AC, Nayak DP, Hama S, Navab M, Fogelman AM. High-density lipoprotein looses its anti-inflammatory properties during acute influenza infection. Circulation. 2001;103(18):2283-8.
  • Kaya MO, Meme kanserli olgularda paraoksonaz (PON1) fenotiplerinin belirlenmesi. Balıkesir Üniversitesi Fen Bilimleri Enstitüsü, Kimya Bölümü Uzmanlık Tezi, Balıkesir 2009.

Prostat Kanserli Hastalarda Oksidatif Stres ve Paraksonaz Aktivite Azalması

Yıl 2015, Cilt: 7 Sayı: 2, 113 - 117, 01.08.2015
https://doi.org/10.18521/ktd.63203

Öz

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)

Kaynakça

  • Engin A, Altan N. Effects of obstructive jaundice on the antioxidative capacity of human red blood cells. Hematologia. 2000;30(2):91-6.
  • 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.
  • 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.
  • Behrend L, Henderson G, Zwacka RM. Reactive oxygen species in oncogenic transformation. Biochem Soc Trans. 2003; 31(Pt 6):1441-4.
  • 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.
  • 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.
  • Mackness MI, Arrol S, Durrington PN. Paraoxonase prevents accumulation of lipoperoxides in low-density lipoprotein. FEBS Lett. 1991; 286:152-4.
  • Greenlee RT, Murray T, Bolden S, Wingo PA. Cancer statistics, 2000. CA Cancer J Clin. 2000; 50(1):7–33.
  • Echerson HW, Wyte CM, La Du BN. The human serum paraoxonase/arylesterase polymorphizm. Am J Hum Genet. 1983; 35(6):1126-38.
  • 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.
  • 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.
  • Akcay MN, Polat MF, Yilmaz I, Akcay G. Serum paraoxonase levels in pancreatic cancer. Hepatogastroenterology. 2003; 50(2):225–7.
  • Akcay MN, Polat MF, Yilmaz I, Akcay G. Serum paraoxonase levels in gastric cancer. Hepatogastroenterology. 2003; 50(2):273–5.
  • 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.
  • 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.
  • Macri A, Versaci A, Loddo S. Serum levels of interleukin 1beta, interleukin 8 and tumour necrosis factor alpha as markers of gastric cancer. Biomarkers. 2006; 11(2):184-93.
  • Van Lenten BJ, Wagner AC, Nayak DP, Hama S, Navab M, Fogelman AM. High-density lipoprotein looses its anti-inflammatory properties during acute influenza infection. Circulation. 2001;103(18):2283-8.
  • Kaya MO, Meme kanserli olgularda paraoksonaz (PON1) fenotiplerinin belirlenmesi. Balıkesir Üniversitesi Fen Bilimleri Enstitüsü, Kimya Bölümü Uzmanlık Tezi, Balıkesir 2009.
Toplam 19 adet kaynakça vardır.

Ayrıntılar

Birincil Dil Türkçe
Bölüm Makaleler
Yazarlar

Orhan N Bu kişi benim

Yayımlanma Tarihi 1 Ağustos 2015
Yayımlandığı Sayı Yıl 2015 Cilt: 7 Sayı: 2

Kaynak Göster

APA N, O. (2015). Prostat Kanserli Hastalarda Oksidatif Stres ve Paraksonaz Aktivite Azalması. Konuralp Medical Journal, 7(2), 113-117. https://doi.org/10.18521/ktd.63203
AMA N O. Prostat Kanserli Hastalarda Oksidatif Stres ve Paraksonaz Aktivite Azalması. Konuralp Medical Journal. Ağustos 2015;7(2):113-117. doi:10.18521/ktd.63203
Chicago N, Orhan. “Prostat Kanserli Hastalarda Oksidatif Stres Ve Paraksonaz Aktivite Azalması”. Konuralp Medical Journal 7, sy. 2 (Ağustos 2015): 113-17. https://doi.org/10.18521/ktd.63203.
EndNote N O (01 Ağustos 2015) Prostat Kanserli Hastalarda Oksidatif Stres ve Paraksonaz Aktivite Azalması. Konuralp Medical Journal 7 2 113–117.
IEEE O. N, “Prostat Kanserli Hastalarda Oksidatif Stres ve Paraksonaz Aktivite Azalması”, Konuralp Medical Journal, c. 7, sy. 2, ss. 113–117, 2015, doi: 10.18521/ktd.63203.
ISNAD N, Orhan. “Prostat Kanserli Hastalarda Oksidatif Stres Ve Paraksonaz Aktivite Azalması”. Konuralp Medical Journal 7/2 (Ağustos 2015), 113-117. https://doi.org/10.18521/ktd.63203.
JAMA N O. Prostat Kanserli Hastalarda Oksidatif Stres ve Paraksonaz Aktivite Azalması. Konuralp Medical Journal. 2015;7:113–117.
MLA N, Orhan. “Prostat Kanserli Hastalarda Oksidatif Stres Ve Paraksonaz Aktivite Azalması”. Konuralp Medical Journal, c. 7, sy. 2, 2015, ss. 113-7, doi:10.18521/ktd.63203.
Vancouver N O. Prostat Kanserli Hastalarda Oksidatif Stres ve Paraksonaz Aktivite Azalması. Konuralp Medical Journal. 2015;7(2):113-7.