الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Doxorubicin is a member of the anthracycline antibiotics. It is a highly utilized antineoplastic drug with high potency against wide range of solid malignancies and hematological tumors. However, the development of drug induced cardiotoxicity has limited its use. where it is capable of causing significant heart toxicity and irreversible cardiomyopathy in medical practice.
Doxorubicin associated damage to cardiac cells is mainly postulated to oxidative stress as the most accepted hypothesis and the key cause. As it is believed that doxorubicin production of oxygen free radicals causes cellular membranes lipid peroxidation and eventually cell damage.
Despite the amount of strategies developed to minimize the devastating effect of doxorubicin on cardiac muscle, its cardiac complication still an obstacle against its beneficial effect as an anticancer drug. thus new drugs are needed to protect against doxorubicin cardiac side effects.
Aldehyde dehydrogenases are among the enzymatic protective mechanisms against oxidative stress. ALDH2 has a crucial role particularly in detoxification of endogenous aldehydes obtained as a result of lipid peroxidation occurring during oxidative stress. Alda-1 functions as an ALDH2 agonist. Through its selective activation of ALDH2, it ameliorates oxidative stress and the raised aldehyde load and subsequently neutralize their damaging effect on cardiomyocytes as well as on the establishment and progression of cardiac diseases.
The purpose of the current work was to shed light on the possible histological alterations that might occur in the left ventricular cardiomyocytes of adult male mice following administration of doxorubicin and the possible protective effect of aldehyde dehydrogenase 2 enzyme activator (Alda-1) with especial emphasis on ultrastructural effects. These changes were also documented by measuring of the body and heart weight as well as by biochemical analysis of cardiac injury biomarkers; Creatinine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) enzymes. Oxidative stress has been suggested to be the main mechanism of toxicity caused by doxorubicin on cardiomyocytes, therefore total antioxidant capacity and toxic aldehyde malondialdehyde were measured.