Lipid peroxidation and antioxidant status in blood and tissue of malignant breast tumor and benign breast disease

Gonenc A., Erten D., Aslan S., Akinci M., Simsek B., Torun M.

CELL BIOLOGY INTERNATIONAL, cilt.30, sa.4, ss.376-380, 2006 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 30 Sayı: 4
  • Basım Tarihi: 2006
  • Doi Numarası: 10.1016/j.cellbi.2006.02.005
  • Dergi Adı: CELL BIOLOGY INTERNATIONAL
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.376-380
  • Anahtar Kelimeler: malondialdehyde, nitric oxide, lipid hydroperoxide, total antioxidant capacity, breast cancer, benign breast disease, OXIDE SYNTHASE ACTIVITY, NITRIC-OXIDE, SERUM, CARCINOGENESIS, ASSOCIATION, CAPACITY, NITRATE
  • Gazi Üniversitesi Adresli: Hayır

Özet

Changes in the levels of malondialdehyde (MIDA), nitrate and nitrite (as an index of nitric oxide production), lipid hydroperoxide (LOH), total antioxidant capacity (TAC), lipids (total cholesterol and triglycerides) and lipoproteins (HDL- and LDL-cholesterol) were estimated in breast cancer patients (n = 15) and benign breast disease (n = 15). Serum and tissue MDA levels were found to be decreased in breast cancer patients compared to the benign group (p < 0.05). In contrast, nitrate and nitrite levels were increased in serum and tissue of the cancer group compared to benign breast disease patients (p < 0.05). Compared to the benign group, tissue TAC levels were elevated in the breast cancer patient group (p < 0.05). Total cholesterol and HDL-cholesterol were elevated in the benign group compared with cancer patients (p < 0.05). These findings support the hypothesis that lipid peroxidation in serum and tissue of benign breast disease is greater than in breast cancer. However, the enhanced levels of nitric oxide may be in response to inflammation in patients with breast cancer. Total antioxidant status is lower in benign tissue than in cancerous tissue, probably to compensate for this elevated free radical production. (c) 2006 International Federation for Cell Biology. Published by Elsevier Ltd. All rights reserved.