Abstract
Urotoxicity is a troublesome complication associated with cylophosphamide (CP) andL-buthionine-SR-sulfoximine (BSO) treatment in chemotherapy. With this concern in mind, this present study investigated the potential effects of diosgenin for the first time on urotoxicity induced by acute CP and BSO doses using a Swiss albino mouse model. Toxicity modulation was evaluated through measuring lipid peroxidation (LPO) and anti-oxidants in urinary bladder. The findings reveal that the diosgenin exerted a protective effect not only on LPO but also on enzymatic anti-oxidants. When compared to the controls, the CP-treated animals underwent significant decrease in the glutathione S-transferase (GST), glutathione reductase (GR), glutathione peroxidase (GP) and catalase (CAT) activities. The level of reduced glutathione (GSH) was also decreased with an increase in LPO in the CP-treated animals. BSO treatment exerted an additive toxic effect in the CP-treated animals. Interestingly, pre-treatment with the diosgenin restored the activities of all enzymes back to normal levels and to exhibit an overall protective effect on the CP and BSO induced toxicities in urinary bladder. The restoration of GSH through the treatment with the diosgenincan play an important role in reversing CP-induced apoptosis and free radical mediated LPO. Key words: Diosgenin, cyclophosphamide, L-buthionine-SR-sulfoximine, urinary bladder anti-oxidants
Highlights
Cyclophosphamide (CP) is one of the most popular alkylating anticancer drugs in spite of its toxic side effects including immunotoxicity, hematotoxicity and mutagenicity
L-Buthionine-Sulfoximine (BSO) is a sulfoximine used in chemotherapy which irreversibly inhibits gammaglutamylcysteine synthetase, thereby depleting cells of glutathione, a metabolite that plays a critical role in protecting cells against oxidative stress and resulting in free radical-induced apoptosis
The findings reveal that BSO treatment brought about a significant increase (P < 0.01) in the lipid peroxidation (LPO) levels in the bladder over the control values (Figure 3)
Summary
Cyclophosphamide (CP) is one of the most popular alkylating anticancer drugs in spite of its toxic side effects including immunotoxicity, hematotoxicity and mutagenicity. CP is an anti-neoplastic agent with activity against a variety of human tumours. It is commonly used as an anti-neoplastic agent for the treatment of various. Several previous studies on murine models have showed that the administration of CP retards the progression of kidney disease (Hengstler et al, 1997). This agent has been used extensively for the treatment of diffuse proliferative glomerulonephritis in patients with renal lupus (Hengstler et al, 1997).
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