الفهرس 
ACKNOWLEDGEMENTSOnly 14 pages are availabe for public view
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Abstract
The anthracycline drug, doxorubicin (DOX) is an antineoplastic agent widely indicated for a variety of cancers. One of its adverse effects is hepatotoxicity which presents with hepatocyte necrosis, sinusoidal dilation, and fibrosis. However, there remains a dearth in this damage’s quantification and zonal distribution. Doxorubicin is widely used to treat leukemias and carcinomas of the breast, lungs, thyroid, and ovary. However, systemic toxicity at clinically relevant doses limits its therapeutic application to some extent. The induction of toxicity is mediated by free radical generation and resultant oxidative stress through two main pathways: A non-enzymatic pathway that utilizes iron and an enzymatic mechanism using the mitochondrial respiratory chain. Due to its biphasic nature, DOX has been shown to induce hepatotoxicity at acute and sub-acute doses. The molecular mechanisms involved in DOX causing hepatotoxicity are mainly due to the production of reactive oxygen species (ROS) by the drug during its metabolism in the liver. These results in imbalanced redox potential leading to oxidative stress, reduced levels of antioxidant enzymes, apoptosis, inflammation, and mitochondrial dysfunction. Drug-induced injury to the liver can mimic any form of acute or chronic liver disease. Acute injury to the liver frequently is due to the action of cytochrome P450, which breaks down drugs into electrophiles or free radicals. So, we aimed to determine whether Se NPs and ZnO NPs can modulate this apoptotic process, potentially alleviating the loss of hepatic cells. Explore whether Se NPs and ZnO NPs exhibit anti-inflammatory properties that could effectively dampen the inflammatory response within hepatic tissues. Assess the effects of zinc oxide and selenium nanoparticles in treating liver damage caused by doxorubicin in rats. The research also aims to investigate whether the combination of selenium and zinc nanoparticles provides better protection against doxorubicin-induced liver toxicity than either component alone or whether this combination offers synergistic benefits that exceed the individual contributions of each component.
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