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العنوان
The protective effects of some drugs on ifosfamide-induced nephrotoxicity /
المؤلف
Moussa, Ethar Abulyazid
هيئة الاعداد
باحث / إيثار أبو اليزيد موسى
مشرف / علاء الدين السيد السيسى
مناقش / وجيه محمود عواره
مناقش / ماجدة السيد الصياد
الموضوع
Pharmacology&toxicology
تاريخ النشر
2012.
عدد الصفحات
p 194. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الصيدلة ، علم السموم والصيدلانيات (المتنوعة)
تاريخ الإجازة
1/1/2012
مكان الإجازة
جامعة طنطا - كلية الصيدلة - اقربازين والسموم
الفهرس
Only 14 pages are availabe for public view

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Abstract

Ifosfamide (IFO) is a structural isomer of cyclophosphamide, was introduced into early clinical trials in 1972 (Pinkerton et aI., 1985). IFO is a prodrug whose biotransformation by hepatic cytochrome P450 isozymes is required (Springate et aI., 1999). Trials have shown it to be a useful drug in the management of several tumors in both pediatrics and adults (Skinner etaI., 1990; Rossi et aI., 1999).IFO causes nephrotoxicity in 30% of paediatric cancer patients, which may present in more sever~ cases as Fanconi syndrome (Skinner et aI., 1993; Loebstein and Koren, 1998) which characterized by a generalized transport defect in the proximal tubules, leading to urinary losses of electrolytes, amino acids, glucose, phosphate, bicarbonate and small molecular weight proteins as well as decrease in glomelular filtration rate (Loebstein et aI., 1999, Rossi et aI., 1999; Skinner, 2003). Alpha lipoic acid (ALA) is a dithiol sulfur containing compound acts as an antioxidant (Kagan et aI., 1992). It reduces oxidative stress by directfree radical scavenging (Roy and Packer, 1998), redox generation of other antioxidants (Packer and Suzuki, 1993; Packer and Witt, 1995), increasing the intracellular glutathion (Kagan et aI., 1992) and restore the activity of antioxidant enzymes, also prevent the increase in lipid peroxidation (Somani et-aI., 2000 and Malarkodi et aI., 2003).Vitamin E act as nonenzymatic antioxidant in the cell membrane. br>Various experimental studies indicated its effectiveness in the prevention of oxidative renal damage (Abdel-Naim et aI., 1999) by direct free radical scavenging, prevention of the decline in renal antioxidant defence system via induction o~ antioxidant enzyme activities (Dillioglugil et aI., 2005; Ajith et