Journals / Medical Network Klinik Bilimler ve Doktor / 2003 / Cilt: 9 - Sayı: 5

Evaluating antioxidant activity in lung cancer

Akciğer kanserinde antioksidan aktivitenin değerlendirilmesi

Pages
569–572
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

In the development of cancer, oxidative stress can play important role, strenghtening of antioxidant capacity can prevent the development of cancer.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objective: Free radicals cause oxidative stress and tjssue damage.
📊
Key Findings & Data:Result: The mean serum levels of SOD, MDA, GSH in patients with lung cancer were 723.4±291.1 Ug/Hb, 7.28±1.83 Umol/L, 5.68±2.65 Umol/gHb respectively.
💡
Conclusion & Impact:In the development of cancer, oxidative stress can play important role, strenghtening of antioxidant capacity can prevent the development of cancer.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Oksidatif stres · Malondialdehit · Akciğer neoplazmları

Abstract

Objective: Free radicals cause oxidative stress and tjssue damage. In tissues with cancer, low levels of antioxidant enzymes and high levels of reactive oxygen metabolites can result with a damage on subcellular organels such as nuclear DNA and cell membrane. Material and Method: To evaluate the role of antioxidant activity, the serum levels of Superoxide dismutase (SOD), Malondialdehyde (MDA) and Glutathion (GSH) are compared in control group and the group with lung cancer. Result: The mean serum levels of SOD, MDA, GSH in patients with lung cancer were 723.4±291.1 Ug/Hb, 7.28±1.83 Umol/L, 5.68±2.65 Umol/gHb respectively. On the control group the mean serum levels of SOD, MDA, GSH were 1164±243.75 Ug/Hb, 4.73±1.95 Umol/L, 4.75±1.29 Umol/gHb respectively. Conclusion: In.our study we found increased oxidative stress in patients with lung cancer. In the development of cancer, oxidative stress can play important role, strenghtening of antioxidant capacity can prevent the development of cancer.

Özet

Amaç: Serbest oksijen radikalleri oksidatif stres ve doku hasarına yol açmaktadır. Kanserli dokularda, antioksidan enzim seviyelerinin düşük, reaktif oksijen metabolitlerinin yüksek olması, hücre membranı ve nükleusunda DNA gibi subselüler yapılarda hasarla sonuçlanabilecek etkilere sebep olabilmektedir. Gereç ve Yöntem: Akciğer kanserinde antioksidan aktiviteyi değerlendirebilmek için süperoksit dismutaz (SOD), malondialdehit (MDA) ile glutatyon (GSH) serum düzeyleri akciğer kanserli ve kontrol grubunda karşılaştırıldı. Bulgular: Akciğer kanserli hastaların ortalama serum SOD düzeyi 723.4±291.1 Ug/Hb, MDA; 7.28±1.83 Umol/L, GSH; 5.68±2.65 Umol/gHb olarak tespit edildi. Kontrol grubunda ise ortalama serum SOD düzeyi 1164±243.75 Ug/Hb, MDA; 4.73±1.95 Umol/L, GSH; 4.75±1.29 Umol/gHb olarak tesbit edildi. Sonuç: Çalışmamızda akciğer kanserli hastalarda oksidatif stresin arttığını tespit ettik. Bu durum bizde akciğer kanser gelişiminde oksidatif hasarın önemli rol oynayabileceği; antioksidan kapasiteyi güçlendirmenin akciğer kanser gelişimini engelleyebileceği düşüncesini oluşturdu.

🔖

Cite This Article

TOPDAĞ, S., CANGEL, U., İLÇE, Z., ÖZAYDIN, İ., ASLANER, A., KAYNAK, M. K. (2003). Evaluating antioxidant activity in lung cancer. Medical Network Klinik Bilimler ve Doktor, Cilt: 9 - Sayı: 5, 569–572. https://ajindex.com/articles/278679

References (14)

  1. Cross CE, Hallivel B, Borish ET, et al. Oxygen radicals and human disease. Ann Int Med. 1987; 107:526-45.
  2. Asayama K, Nakane T, Uchida H, Hayashibe K, Dobashi K, Nakazawa S. Serum antioxidant status in streptazosin-induced diabetic rat. Metab Res 1994; 26:617-20.
  3. Corrocher R, Casaril M, Bellisola G, et al. Severe impairment of antioxidant system in human hepatoma. Cancer 1986; 58:1658-62.
  4. Mantha SV, Prasad MJ, Prasad K. Antioxidant enzymes in hypercholesterolemia arid effects of vitamin E in rabbits. Atherosclerosis 1993; 101:135-44.
  5. McCay RN, Hill KE, Ayon MA, Stein JH, Burk RF. Oxidant stress following renal ischemia: Changes in the glutathione redox ratio. Kidney int 1988; 33:812-7. Yalçın S. Antioksidanlar. Klinik Gelişim 1998; 11:342-6.
  6. Cotran RS, Kumar V, Robbins SL. Cellular injury and cellular death. İn: Schoen FJ, ed. Patholologic basis of disease, 5th ed. London: WB saunders; 1994:1-34. Fridovich I. Superoxide dismutases. Adv Enzymol 1986; 586:61-4.
  7. Bolann BJ, Ulvik RJ. Improvment of a direct spectrophoto- metric assay for routine determination of superoxide dismutase activity. Clin Chem 1991; 37:1993-9.
  8. Bannister JV, Bannister WH, Rutilio G. Aspects of the structure, function and applications of superoxide dismutase. Crit Rev Biochem 1987; 22:111 -80. Sun Y. Free radicals, antioxidant ezymes and carcinogenesis. Free radic Biol Med 1991; 8:538-99.
  9. Zhang H, Agardh E, Agardh C. Nitroblue tetrazolium staining: a morphological demonstration of superoxide in the rat retina. Graefe's Arch Clin Exp Ophthalmol 1993; 231:178-83. 0berly LW, Buetner GR. Role of superoxide dismutase in cancer: a review. Cancer Res 1979; 39:1141-9.
  10. Peksin AV, Zbarsky IB, Konstantinov AA. An examination of the superoxide dismutase activity in tumor tissue. Dokl Akad Nauk 1976; 229:751-4.
  11. Oberley LW, Bize IB, Sahu. Superoxide dismutase activity of normal murine liver.regenerating liver, and H6 hepatoma. J Natl Cancer Inst. 1978; 61:375-9.
  12. Jaruga P, Zastawny TH, Skokowski S. Oksidative DNA base damage and antioxidant enzyme activities in human lung cancer. FEBS Lett 1994; 341:59-64.
  13. Sun Y, Oberley LW, Li Y. A simple method for clinical assay of superoxide dismutase. Clin Chem 1988; 34:497-500.
  14. Aydın M, Güler O, Sekeroğlu R. Comparison of serum and malignant tissue MDA levels in patients with gastrointestinal malignancies. JIMA 1999; 31:156-8.