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Pharmacological study of the possible protective effects of some antioxidants and trace elements on cisplatin-induced nephrotoxicity in rats / Kamel Mohamed Kamel ; Supervised Mostafa E. Elsayed , Hekma A. Abdellatif , Salwa A. Metwally

By: Contributor(s): Material type: TextTextLanguage: English Publication details: Cairo : Kamel Mohamed Kamel , 2015Description: 243 P. : charts , photographs ; 25cmOther title:
  • دراسة دوائية للتداخلات المحتملة للتأثيرات الوقائية لبعض مضادات أكسدة و عناصر نادرة علي التسمم الكلوى المحدث بمادة سيسبلاتين في الجرذان [Added title page title]
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  • Issued also as CD
Dissertation note: Thesis (M.Sc.) - Cairo University - Faculty of Pharmacy - Department of Pharmacology and Toxicology Summary: Drug-induced nephrotoxicity is an extremely common condition and is responsible for a variety of pathological effects on the kidneys. Cisplatin (CIS), one of the most effective and potent anticancer drugs, is used in the treatment of a wide variety of both pediatric and adult malignancies. However, the chemotherapeutic use of cisplatin is limited by its serious side-effects, such as nephrotoxicity and ototoxicity. The present study was performed to elucidate some of the mechanisms involved in the nephroprotective effects of selenium, onion oil, hesperidin and rutin in experimentally cisplatin-induced nephrotoxicity in rats. Cisplatin induced nephrotoxicity was confirmed by elevated serum sodium, total sodium and potassium excreted in urine, serum creatinine, urinary creatinine, BUN, urine volume and relative kidney weight and decreased serum potassium and creatinine clearance. Cisplatin also enhanced caused lipid peroxidation manifested as: decrease in the activity of the antioxidant enzyme (SOD), significant depletion of GSH, enhancement of MDA production in the renal tissue and caused degenerative changes, diffuse acute tubular necrosis, focal inflammatory cells infiltration and focal haemorrhage associated with tubular cast formation. Selenium, onion oil, hesperidin or rutin hampered CIS-induced nephrotoxicity manifested by an enhancement of the glomerular filtration rate which was associated by the reduction of serum sodium, total sodium and potassium excreted in urine, serum creatinine, urinary creatinine, BUN, urine volume and relative kidney weight
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Thesis Thesis قاعة الرسائل الجامعية - الدور الاول المكتبة المركزبة الجديدة - جامعة القاهرة Cai01.08.09.M.Sc.2015.Ka.P (Browse shelf(Opens below)) Not for loan 01010110067400000
CD - Rom CD - Rom مخـــزن الرســائل الجـــامعية - البدروم المكتبة المركزبة الجديدة - جامعة القاهرة Cai01.08.09.M.Sc.2015.Ka.P (Browse shelf(Opens below)) 67400.CD Not for loan 01020110067400000

Thesis (M.Sc.) - Cairo University - Faculty of Pharmacy - Department of Pharmacology and Toxicology

Drug-induced nephrotoxicity is an extremely common condition and is responsible for a variety of pathological effects on the kidneys. Cisplatin (CIS), one of the most effective and potent anticancer drugs, is used in the treatment of a wide variety of both pediatric and adult malignancies. However, the chemotherapeutic use of cisplatin is limited by its serious side-effects, such as nephrotoxicity and ototoxicity. The present study was performed to elucidate some of the mechanisms involved in the nephroprotective effects of selenium, onion oil, hesperidin and rutin in experimentally cisplatin-induced nephrotoxicity in rats. Cisplatin induced nephrotoxicity was confirmed by elevated serum sodium, total sodium and potassium excreted in urine, serum creatinine, urinary creatinine, BUN, urine volume and relative kidney weight and decreased serum potassium and creatinine clearance. Cisplatin also enhanced caused lipid peroxidation manifested as: decrease in the activity of the antioxidant enzyme (SOD), significant depletion of GSH, enhancement of MDA production in the renal tissue and caused degenerative changes, diffuse acute tubular necrosis, focal inflammatory cells infiltration and focal haemorrhage associated with tubular cast formation. Selenium, onion oil, hesperidin or rutin hampered CIS-induced nephrotoxicity manifested by an enhancement of the glomerular filtration rate which was associated by the reduction of serum sodium, total sodium and potassium excreted in urine, serum creatinine, urinary creatinine, BUN, urine volume and relative kidney weight

Issued also as CD

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