Long term administration of granulocyte-macrophage colony stimulating factor decreases development of 1-2 dimethylhydrazine-induced colon cancer in rats

Dinc S., Ozbirecikli B., Kuru B., GÜLÇELİK M. A., Ustun H., Alagol H., ...Daha Fazla

Journal of Surgical Oncology, cilt.95, sa.1, ss.12-21, 2007 (SCI-Expanded, Scopus)

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 95 Sayı: 1
  • Basım Tarihi: 2007
  • Doi Numarası: 10.1002/jso.20540
  • Dergi Adı: Journal of Surgical Oncology
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.12-21
  • Anahtar Kelimeler: granulocyte-macrophage colony stimulating factor, dimethylhydrazine, colon cancer, free radicals, nitric oxide
  • Sağlık Bilimleri Üniversitesi Adresli: Evet

Özet

Background and Objectives: The antitumoral activities of granulocyte-macrophage colony stimulating factor (GM-CSF) were shown earlier. In this study, the effects of GM-CSF were investigated on colon cancer induced by 18 weeks of 1-2 dimethylhydrazine (DMH) administration in rats. Methods: Four groups received subcutaneous saline (n = 20), 15 mg/kg DMH (n = 30), DMH +6 μg/kg GM-CSF (n = 30), and DMH +12 μg/kg (n = 30) GM-CSF. Results: The average number of tumors (2.8 vs. 1.5) and mean tumor volume (179 ± 36 vs. 27 ± 9 mm3; means ± SEM) were reduced in DMH + GM-CSF groups as compared to the DMH group (n = 30, P < 0.01). DMH-induced enhancement of free radicals and lipid peroxidation were decreased in DMH + GM-CSF group (n = 8-12, P < 0.05). The magnitude of DMH-induced alterations in superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities was lowered in the DMH + GM-CSF group (n = 12-16, P < 0.05). DMH-induced increases in the total nitrite/nitrate levels and the nitric oxide synthase (NOS) activity (n = 10-12, P < 0.05) were also reduced in the DMH + GM-CSF group (n = 8-9, P < 0.05). Conclusions: The results indicate that GM-CSF inhibits the development of DMH-induced colon cancer in rats and suggest that inhibition of oxidative stress and NO pathway are involved in the observed antitumoral effects. © 2006 Wiley-Liss, Inc.