الفهرس 
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Abstract
Aspirin is one of NSAIDS which is widely used therapy from thousand years ago. It is used for relieving pain and reducing fever in adult by exerting its anti-inflammatory, analgesic and antipyretic actions. NSAIDS manifest identical toxic actions on gastric mucosa and kidney. It has been reported that aspirin induced liver cell damage.
The present study was designed to investigate the effect of aspirin on the liver of Swiss albino mice using histological, cytological, histochemical and ultrastructural techniques.
Mice were divided into 2 groups, control group received saline as vehicle and experimental group received 100 mg aspirin/ kg body weight 3 times a week for 1 month.
1- Histological findings
Histological examination of Haematoxylin and Eosin sections of mice liver which received aspirin revealed hemorrhage in the liver sinusoids and portal tract in addition to presence of inflammatory cells after 7 days administration. After 15 days of aspirin administration apoptotic figure were noted in addition to inflammation. 21 days later there was area of inflammatory cells around the congested portal tract. Some cells showed nuclear disintegration and apoptotic figures in others. After 30 days the nuclear disintegration was increased in addition to the presence of fatty liver, inflammation, apoptosis and congestion.
2- Electron microscopic findings
Early signs of apoptosis including ring condensation of nuclear chromatin along the nuclear envelope which appeared as dense clumping chromatin by increasing the drug administration. There are also early swelling mitochondria with electron lucent matrix that finally showed complete mitochondrial damage. Interrupted and shortening of RER can be easily recognized in addition to increased in glycogen deposits and lipid DROPlets.
3- Histochemical findings
A- Glycogen
Using PAS stain, glycogen in all liver cells was recognized as red homogenous granules in marked grade intensity either in normal or even 7 days post aspirin administration. After 15 days later the intensity of glycogen increased to be strong . Kupffer cells and apoptotic bodies also showed positive stain. 21 days later some cells showed weak grade PAS and moderate in Kupffer cells while other showed strong PAS, 30 days later there was a depletion in PAS to be moderate in almost liver cells.
B- Superoxide dismutase (SOD)
The activity of SOD was noted using hypoxanthine-cerium DAB technique as insoluble blue product distributed in the cytoplasm. The activity of SOD was gradually increased starting from 7 to 30 days from grade marked to strong respectively. This activity of SOD post aspirin administration was dose- dependent.
Conclusions
Hepatotoxicity related to NSAIDs is an uncommon adverse effect, it is important to be vigilant to the hepatotoxicty potential of any NSAID, as increased awareness and reporting of theses events will lead to a better understanding of the risk factors and the pathophysiology of NSAID- related hepatotoxicity. These result suggest that aspirin administration must be under restruction and control especially for patient with liver disease.