الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Chemotherapy medications have a wide range of side effects since they are cytotoxic and non-specific. In order to minimize the side effects of
hemotherapies, treatment methods have been improved by a combination of medicines with various molecular targets. Doxorubicin (DOX) has long been a cornerstone of several forms of cancer therapy. Despite having idespread anticancer action, aditional DOX’s usage in clinical practice has been
lonstrained by side effects, especially hepatotoxicity and cardiotoxicity. Biguanides, Metformin (Met) remains the first-line treatment option or most diabetic patients. Met increases insulin sensitivity, suppress the production of glucose in liver tissues, promotes fatty acid oxidation, lowers gastrointestinal glucose absorption, and improves glucose uptake via phosphorylating the GLUT-enhancer factor. Furthermore, pre-clinical and clinical studies showed that Met has a potential role to lower the diovascular complications in the diabetic and non-diabetic patients. The current investigation aimed to address the Met impact’s molecular and biochemical mechanisms on DOX-induced oxidative stress in male Sprague Dawley rats and to explore whether the antioxidant enzyme has the potential to increase its activity, regardless of its quantity or whether its activity is due to its gene expression. Forty rats were equally divided into four groups; group I was the negative control group; rats were injected intraperitoneally (i.p) with saline in a proportional volume and in the same time scheme of other experimental groups. group II were injected with DOX (4 mg/kg) i.p. twice a week for 14 days. group III were injected with Met (250 mg/kg) by gavage daily for 14 days.