IADR Abstract Archives
The effect of α-glucosyl hesperidin on oral mucositis induced by treatment of 5-fluorouracil with acetic acid.
Objectives: We examined the biological functions of a-glucosyl hesperidin (Hsp-G) on oral stomatitis.
Methods: The scavenge activity of Hsp-G on reactive oxygen species was measured by electron spin resonance spectroscopy. An oral mucositis animal model induced by treatment of 5-fluorouracil (5-FU) with 10% acetic acid in hamster cheek pouch was used. The oral mucositis group and Hsp-G pre-treatment group were administered an intraperitoneal injection of 5-FU on days 0 and 2 of the experiment at a dose of 60 mg/kg body weight. All animals were observed and weighed on days 0, 1, 2, 3, 4, 7, 9, 11, 14, and 16. Hamsters were anesthetized for observations, the left side cheek pouch was everted, and a clinical photograph of oral mucositis was taken with a digital camera. A free computer program (Image J) was used to measure the area of mucositis as cm2. Lipid peroxidation was measured as the level of malondialdehyde determined by the thiobarbituric acid reaction. The protocols were approved by Institutional Animal Care Committees. Human oral squamous carcinoma (HSC-3) cells were cultures for determination of 5-FU-induced inhibition of cell growth in the presence of Hsp-G.
Results: Hsp-G exhibited scavenging activity toward hydroxyl radical and superoxide. Oral stomatitis areas were significantly smaller in hamsters administered Hsp-G than in the non-administration group. Increases in thiobarbituric acid reactive substances, expressed as malondialdehyde equivalents, levels were significantly inhibited by the pre-treatment with Hsp-G prior to the administration of 5-FU. Hsp-G had no effect on anti-tumour activity in human oral squamous carcinoma cells.
Conclusions: The pre-administration of Hsp-G inhibited the exacerbation of oral mucositis as a side effect of cancer chemotherapy without affecting the anti-tumour activity of 5-FU. These results indicate the potential of Hsp-G to reduce the clinical disadvantages associated with 5-FU in cancer patients.
Methods: The scavenge activity of Hsp-G on reactive oxygen species was measured by electron spin resonance spectroscopy. An oral mucositis animal model induced by treatment of 5-fluorouracil (5-FU) with 10% acetic acid in hamster cheek pouch was used. The oral mucositis group and Hsp-G pre-treatment group were administered an intraperitoneal injection of 5-FU on days 0 and 2 of the experiment at a dose of 60 mg/kg body weight. All animals were observed and weighed on days 0, 1, 2, 3, 4, 7, 9, 11, 14, and 16. Hamsters were anesthetized for observations, the left side cheek pouch was everted, and a clinical photograph of oral mucositis was taken with a digital camera. A free computer program (Image J) was used to measure the area of mucositis as cm2. Lipid peroxidation was measured as the level of malondialdehyde determined by the thiobarbituric acid reaction. The protocols were approved by Institutional Animal Care Committees. Human oral squamous carcinoma (HSC-3) cells were cultures for determination of 5-FU-induced inhibition of cell growth in the presence of Hsp-G.
Results: Hsp-G exhibited scavenging activity toward hydroxyl radical and superoxide. Oral stomatitis areas were significantly smaller in hamsters administered Hsp-G than in the non-administration group. Increases in thiobarbituric acid reactive substances, expressed as malondialdehyde equivalents, levels were significantly inhibited by the pre-treatment with Hsp-G prior to the administration of 5-FU. Hsp-G had no effect on anti-tumour activity in human oral squamous carcinoma cells.
Conclusions: The pre-administration of Hsp-G inhibited the exacerbation of oral mucositis as a side effect of cancer chemotherapy without affecting the anti-tumour activity of 5-FU. These results indicate the potential of Hsp-G to reduce the clinical disadvantages associated with 5-FU in cancer patients.