The effect of granulocyte macrophage-colony stimulating factor on the prostaglandin E2-like activity of the small intestine of rat during total body irradiation

• Published in: Prostaglandins, leukotrienes and essential fatty acids leukotrienes and essential fatty acids, 2000-06, Vol.62 (6), p.349-353
• Main Authors: Kilic, D., Sayan, H.
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; Diseases of the digestive system; Medical sciences; Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects)
• ISSN: 0952-3278; 1532-2823
• DOI: 10.1054/plef.2000.0165

Radiation-induced gastrointestinal toxicity is important for subjects receiving radiation to the pelvis. Eicosanoids and free radicals may be involved in the mechanism. rHuGM-CSF is a subcutaneously administered drug which may reduce some side effects of radiation. This experimental study was undertaken to determine the effectiveness of rHuGM-CSF on PGE2-like activity of the small intestine in rats. Thirty-two adult male Wistar-Albino rats entered the study to be randomized to one of the four groups: Group I. Control; II. Drug administered; III. Irradiated; IV. Irradiated and drug administered. Radiation was by total body irradiation, 800 rads with Cobalt 60. On the 9th day the animals were killed and biopsies were taken from the terminal ileum. PGE2-like activity was evaluated. Animals were weighed on the day of irradiation and end of the experiment. A statistically significant difference was found according to pre- and post-treatment weights in the irradiated and nonirradiated drug administered groups (Groups II and IV) (P=0.035 and 0.018, respectively). PGE2-like activity in the intestinal tissue was statistically significant higher in the drug-treated animals, both in non-irradiated and irradiated groups. Surprisingly, irradiation was found to decrease the PGE2-like activity in the intestinal tissue (P=0.008). rHuGM-CSF was found to increase PGE2-like activity in the intestinal tissue. The cellular mechanisms underlying this must be clearly determined and weighed carefully in considering the drug for clinical usage.