الفهرس 
Anatomy of the liverذOnly 14 pages are availabe for public view
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Abstract
Cyclophosphamide (CPA) is a versatile anticancer drug that has demonstrated efficacy against a wide range of malignancies and autoimmune disorders. However, it has a range of adverse effects, including bone marrow suppression, hepatotoxicity, cognitive impairments, bladder toxicity and nephrotoxicity. The anti-cancer activity of CPA is attributed to phosphoramide mustard, while acrolein is responsible for its toxic side effects. Acrolein disrupts cellular antioxidant defenses, generating highly reactive free radicals, and exhibits mutagenic properties in mammalian cells. The exact mechanisms underlying CPA-induced liver damage remain elusive; however, accumulating evidence suggests that oxidative stress, an exaggerated inflammatory response, and an apoptotic cascade are likely the key contributors to hepatic injury. Accordingly, this study aims to evaluate the possible protective effects of Trifluoperazine (TFP), a commonly prescribed antipsychotic drug, against CPA induced hepatotoxicity. Also, to explore the emerging activation of autophagy via AKT/mTOR and Nrf2/HO-1 signaling pathways that may be involved in the potential protective effects on CPA induced hepatotoxicity. To achieve these goals, hepatotoxicity was experimentally induced by a single I.P. injection of CPA (200 mg/kg) on day 7. Adult male swiss albino mice were randomly allocated into four groups (8 mice each): • Control group: animals received normal saline (I.P.) for seven consecutive days.