الفهرس 
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Abstract
Cyclophosphamide is an anti- cancer drug, used in chemotherapy. This is a toxic drug which targets the cancer cells and also the normal cells of the body. The original compound is inactive in vitro and exercises its biologic action through metabolites, chiefly phosphoramide mustard and acrolein.
The objective is to study the harmful effects of this drug on liver and bone marrow histology of adult albino rats and also the possible protective effect of captopril.
In the present study, 60 adult albino rats were used and they were divided into 4 groups; the first group (the control group). The second group (Captopril group) was given captopril (capoten tablet 50m /kg daily for 5 days orally).The third group (Cyclophosphamide group) was given a single high dose of CYC by intraperitoneal injection (150mg/kg). The fourth group (CYC+ captopril group) was given CYC (single dose 150 mg/kg i.p.) after captopril (50 mg/kg daily for 5 days p.o).
24 hours after the last injection, rats in all groups were killed and the liver and bone marrow tissues of rats were collected for further analyses (light &electron microscopy).
The biochemical study demonstrated that there was as a significant increase in the serum levels of ALT&AST in group 3 treated with cyclophosphamide. However, group 4 treated with a combination of Captopril with CYC there was slight decrease in the measured parameters.
In addition, blood samples from CYC-intoxicated group, revealed that the hemoglobin level, white blood cell, and platelet counts were significantly decreased compared to the control group.
Fortunately, group 4 treated with a combination of Captopril with CYC revealed a less decrease in the level of hemoglobin, white blood cell, and platelet counts.
The light microscopical study of the liver showed histological changes These changes were represented by congestion of the central veins and the blood sinusoids and also congestion of the portal veins. The hepatocytes were also exposed to degenerative changes in the form of the appearance of vacuoles in the cytoplasm; pyknotic nuclei and apoptosis of some cells. There was also inflammatory cell infiltration.
The light microscopical study of the bone marrow of rats showed hypocellular bone marrow and increase adipose tissue significantly in the group received CYC. However, administration of captopril prior to CYC improved the microscopic picture.
The electron microscope examination of liver reviled that cyclophosphamide cause cell injury by oxidative stress this is appear in the form of Swelling and vacuolization of mitochondria, degeneration of nuclear membrane and accumulation of lipid globules. Pretreatment with captopril markedly reduced these changes.
Conclusion:
Our study indicated that CYC induced hepatotoxicity, bone marrow suppression and hematological disturbances. These alternations were ameliorated upon treatment with captopril as it has antioxidant, hepatoprotective and myeloprotective effects.