Abstract
BackgroundCisplatin (CIS) is a potent antineoplastic agent with high therapeutic efficacy against many kinds of tumors. Its use is limited by its nephrotoxicity. The aim of this work was to minimize cisplatin effective dose and the possible reduction of its severe side effects. The present study was designed to assess the role of sulfur containing agent dimethyl sulfoxide (DMSO) on sensitization of mammary carcinoma, Ehrlich ascites carcinoma (EAC), to the action of cisplatin and at the same time the possible protective effect against cisplatin induced nephrotoxicity in experimental animals.MethodsTo evaluate these effects we have explored the cisplatin effect on the survival time of tumor-bearing animals, tumor weight, cisplatin cellular uptake, apoptosis induction and cell cycle distribution and renal function in presence and absence of DMSO.ResultsCisplatin at dose of 4.5 mg/kg increased the mean survival time of tumor bearing mice to 37 days compared with tumor bearing control mice. Pretreatment of tumor bearing mice with DMSO 50 % (2 ml/kg equal to 1 gm/kg) 2 h. before cisplatin showed a significant increase in their mean survival time 43 days compared to cisplatin treated animals. DMSO pretreatment retained rat’s serum urea and creatinine levels to normal compared to animals treated with cisplatin alone.ConclusionDMSO pretreatment enhanced the cytotoxic activity of cisplatin against the growth of EAC in vivo and showed protective effects against cisplatin-induce nephrotoxicity.
Highlights
Cisplatin (CIS) is a potent antineoplastic agent with high therapeutic efficacy against many kinds of tumors
Osman et al Cancer Cell Int (2015) 15:104 as dimethyl sulfoxide (DMSO) could enhance cisplatin cytotoxicity by facilitating cisplatin entry into cells, increasing its intracellular concentration and likelihood of binding to DNA. In light of these findings the goal of this study is to examine the possible effect of DMSO pretreatment in enhancing the antitumor activity of CIS by examining CIS antitumor activity, apoptosis induction, cell cycle distribution and cisplatin cellular uptake into tumor cells
Assessment of tumor weight Ehrlich ascites carcinoma cells were collected from the ascitic fluid of female Swiss albino bearing mice 8–10 days old ascites tumor. 1 × 106 EAC cells were injected intramuscularly in right thigh of female Swiss albino mice selected for the experiment on day 0
Summary
Cisplatin (CIS) is a potent antineoplastic agent with high therapeutic efficacy against many kinds of tumors. Cisplatin is one of the most active cytotoxic agents in clinical use that has proven efficacy against numerous human solid malignancies such as bladder, cervical, head and neck, esophageal, and small cell lung cancer [1]. Some tumors such as colorectal and non-small cell lung cancers have intrinsic resistance to cisplatin, while others such as ovarian or small cell lung cancers develop acquired resistance after the initial treatment [2]. Uribe et al [8], found that DMSO treatment potentiated the effect of cisplatin and killed more sensory hair cells than treatment with cisplatin alone
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