Effects of the Paciltaxel and Radiation in the Mucosa of the Small Bowel of Rat.
- Author:
Kyung Ja LEE
1
Author Information
1. Department of Therapeutic Radiology, Ewha Womans University, College of Medicine, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Paclitaxel;
Radiation;
small bowel;
Mitotic arrest;
Apoptosis
- MeSH:
Abdomen;
Animals;
Apoptosis;
Cell Cycle;
Incidence;
Infusions, Parenteral;
Kinetics;
Mitosis;
Mucous Membrane*;
Paclitaxel;
Rats*
- From:Journal of the Korean Society for Therapeutic Radiology
1996;14(4):255-264
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Paclitaxel is a chemotherapeutic agent with potent microtublue stablelizing activity that arrests cell cycle in G2-M. Because G2-M is the most radiosensitive phase of the cell cycle. Paclitaxel has potential as a cell cycle- specic radio sensitizer. This study was design to investigate the ablity of paclitaxel to increase the radiotoxicity in normal small bowl mucosa of the rat. METHODS AND MATERIALS: A single intraperitoneal infusion of paciltaxel(10mg/kg). And a single irradiation(8 Gy, x-ray) to the whole abdomen and combination of radiation(8 Gy, x-ray) 24 hours after paclitaxel infusion in the rats were done. The changes of jejunal mucosa. And kinetics of mitotic arrest and apoptosis in the jejunal crypt were defined at 6 hours – 5 days after each treatment histologically. RESULTS: Paclitaxel blocked jejunal crypt cell in mitosis and induced minmal apoptosis. Mitotic arrest by paclitaxel was peaked at 6 hours after infusion and returned to normal by 24 hours. Radiation induced apoptosis and peaked at 6 hours and returned to normal by 24 hours. Combination of paclitaxel and radiation blocked crypt cell in mitosis at 3 days and induced apoptosis slightly at 6 hours and 24 hours and returned to normal by 3 days. The incidence of apopsis in combined group at 6hours was slightly higher than normal control buy significantly lower than radiation alone group. The major changes of jejunal mucosa were nuclear vesicle and atypia which were appered at 6 hours – 3 days and returned to normal by 5 days. The degree of mucosal changes are no different in 3groups except for absence of inflmatory reaction in radiation group. CONCLUSION: Mitotic arrest by paclitaxel was peaked at 6hours and returned to normal by 24 hours and paclitaxel induced minimal apoptosis. Radiation induced apoptosis. Peaked at 6 hours and returned to normal by 24 hours. Radiation induced apoptosis was less in combined group which suggested that paclitaxel have a radioprotective effech when radiation was given 24 hours after paclitaxel infusion.
