Abstract
The goal of this study was to determine the possible beneficial effect of olive oil (7 g/kg) with fig (1 g/kg) and date palm fruit (1 g/kg) extracts (OFD) on the toxicity hazards of doxorubicin (DOX) and (or) γ-radiation. The DOX-treated groups received doses of 2.5 mg/kg body weight via intravenous (IV) injection weekly for four consecutive weeks. Rats in the irradiated groups were exposed to whole-body γ-radiation with fractioned doses of 2 Gy weekly for four consecutive weeks. The OFD-treated groups received two weeks of pretreatment with OFD and daily supplementation via oral gavage during the experimental period. The DOX-treated and (or) irradiated groups showed decreases in the antioxidant parameters (reduced glutathione and nitric oxide) as well as increased lipid peroxidation products. In addition, we observed changes in the lipid profile parameters, lipid risk ratios, and hematological values (erythrocyte (RBC) count, hemoglobin (Hb) concentration, hematocrit (Hct) percentage, platelet count, and total and differential leukocyte (WBC) count) in these groups compared with the control rats. The administration of OFD to DOX-treated and (or) irradiated rats significantly ameliorated the oxidative stress markers, lipid profile, risk ratios, and hematological parameters. In conclusion, OFD could be used synergistically to decrease the negative side effects of chemotherapy and radiotherapy.
Highlights
Doxorubicin (DOX) is an anthracycline antineoplastic drug[1]
Each rabbit was treated with a single dose of DOX (Ebewe Pharma, Austria) (25mg/kg/i.p.) at the day 3; these animals were sacrificed at the day 5
The nephrotoxic effect of DOX characterized by decreasing glomerular filtration rate that leading to a rise in serum urea and creatinine
Summary
Doxorubicin which is essential in treating breast and oesophageal carcinomas, solid tumors in childhood, osteosarcomas, Kaposi’s sarcoma, soft tissue sarcomas, and Hodgkin and non-Hodgkin lymphomas[2]. Doxorubicin activation of stressrelated signaling pathways and cytokines receptors causes an imbalance between the pro-apoptotic and antiapoptotic factors; this imbalance will increase the permeability of mitochondrial membrane, enhance the release of cytochrome C oxidase, prolong the opening time of calcium channels in the sarcoplasmic reticulum, and end with cell death[9]. PTX had been reported to suppress the production of tumor necrosis factor-alpha (TNF-α) and modulate the production of other inflammatory cytokines[10]. It has the potential to decrease intraglomerular pressure and there was an early interest in pentoxifylline as a therapeutic agent in patients with kidney disease[13]
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