Histochemical study on the possible effect of acetyl salicylic acid [aspirin] on the percentage of survival cells in salivary glands of irradiated rat

ABSTRACT

In this report the protective effect of acetyl salicylic acid [ASA] against radiation injury to salivary glands in rats was assessed. Thirty male rats were used in this study and classified as two groups. The control group didn't receive ASA throughout the experiment. While the experimental group received ASA in drinking water [2.5g/ 1L] one week before the exposure to irradiation. Both groups were irradiated by single dose gamma radiation [6.5Gy]. The administration of ASA to the experimental group was continued up to five weeks after radiation. The parotid and submandibular salivary glands were excised and prepared for histological and histochemical examination. The prepared sections were either stained with Haematoxylin and Eosin for routine histological examination, while others were stained by silver staining for detection of Nucleolar Organizer Region [AgNORs] at one and five weeks only. Our data revealed remarkable reduction in the damaged effect of irradiation in the experimental group of both glands along all period of the experiment following irradiation. Furthermore, the regeneration rate of destructive parenchymal elements was found to be faster in the experimental group than in the control group. By employing silver staining to detect the nucleolar organizer region, our results reported that the survival cells were stained brown. Comparing the whole results, it was obvious that the percentage of survival cells were higher in the parotid gland than in the submandibular gland. Furthermore the experimental group of both glands showed significant increase in the survival cells as well as in their distribution compared to that observed in the control group both after one and five weeks following irradiation. Finally the protective effect of ASA reflected on the higher percentage of survival cells in the experimental group in both glands. This could be explained on the assumption that ASA produced a concentration dependent reduction in radiation induced DNA damage in the cells