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Egypt. J. Exp. Biol. (Zoo.). 2009; 5(0): 115-121


Eman A. Youssef, Abdel- AA. Ismail, Ashour A. Abdel-Mawla, Rasha M. Nafei.

The mechanism, by which acetyl salicylic acid causes liver cell damage, remains obscure. The present work was conducted to investigate the changes of hepatocytes resulted post aspirin administration. Fifty two male Swiss albino mice were used. Forty mice were orally received 100 mg aspirin/Kg BW, three times a week for one month. Mice were sacrificed after 7, 15, 21, and 30 days and liver specimens were subjected to routine histological staining, histochemical study of the antioxidant enzyme superoxide dismutase (SOD) and ultrastructure study. Histologically the results indicated that seven, fifteen and twenty one day post aspirin administration revealed congestion in sinusoids, central vein and portal tracts. Moreover, inflammation, vacuolization and nuclear disintegration were illustrated after 15 days and onwards. These histological changes were early explored at ultrastructural level by electron microscope. Ring condensation of nuclear chromatin, swelling and electron lucent matrix of mitochondria and shortening of rER were observed after 7 days. Electron microscopic changes were time dependant where damaged mitochondria, prominent lipid droplets and damaged rER were obvious at 30 days. Histochemically, SOD exerted its activity in the cytoplasm and gradually increased starting from 7 to 30 days. It was shown that although SOD increased, apoptosis increased. This may be a suggestion that reactive oxygen species (ROS) haven't a primary role in apoptosis induced by aspirin.

Key words: Ultrastructure, histology, SOD, aspirin, mice and hepatocytes

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