Pharmacology lettersEvidence of renal metabolism of ifosfamide to nephrotoxic metabolites
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Tinospora cordifolia ameliorates urotoxic effect of cyclophosphamide by modulating GSH and cytokine levels
2012, Experimental and Toxicologic PathologyCitation Excerpt :It is not cytotoxic by itself but undergoes activation through a metabolic step In vivo. Numerous metabolites are known (Woodland et al., 2000; Kerbusch et al., 2001) and the major ones are chloroethylazairidin, acrolein and 4-hydroxy cyclophosphamide produced by the mixed function of cytochrome p450 oxidase present in hepatic microsomes (Dumontet et al., 2001). These metabolites are excreted in the urine.
Comparative metabolism of cyclophosphamide and ifosfamide in the mouse using UPLC-ESI-QTOFMS-based metabolomics
2010, Biochemical PharmacologyCitation Excerpt :The current findings suggest that IF-induced side effects may result directly from CAA rather than from SCMC and TDGA. Studies have reported that CAA can result in neurotoxicity and nephrotoxicity [50,51]. This observation may offer one potential mechanism to explain IF-related neurotoxicity and nephrotoxicity.
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2009, Genetic Diseases of the KidneyMorin mitigates ifosfamide induced nephrotoxicity by regulation of NF-kappaB/p53 and Bcl-2 expression
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