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العنوان
Possible Protective Effect of Telmisartan Versus Captopril on Doxorubicin-induced Cardiac Toxicity and Nephrotoxicity in Rats /
الناشر
Yasmine Farouk Abd El-Nasser,
المؤلف
Abd El-Nasser, Yasmine Farouk.
هيئة الاعداد
باحث / Yasmine Farouk Abd El-Nasser
مشرف / Hussien Ismail Ahmed El-Bitar
مشرف / Osama Mohammed Ashour
مشرف / Mohammed Abd Ellah Ibrahim
الموضوع
Pharmacology. Nephrotoxicity. Telmisartan. Captopril.
تاريخ النشر
2009 .
عدد الصفحات
231 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
علم الأدوية (الطبية)
تاريخ الإجازة
1/1/2009
مكان الإجازة
جامعة المنيا - كلية الطب - Basic Medical Sciences (Pharmacology)
الفهرس
Only 14 pages are availabe for public view

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Abstract

The main objective of the present study is to investigate the possible protective effects of the angiotensin receptor blockers ”telmisartan” versus the angiotensin converting enzyme inhibitor ”captopril” against cardio- and nephro-toxicity induced in rats by the cytotoxic agent doxorubicin (six equal doses 2.5 mg/kg/48 hours). Results of the second set of experiments indicated that induction of cardiac and nephrotoxicities by DOX in rats was accompanied with significant increase in MDA; the marker of lipid peroxidation and decrease with activity of the antioxidant defense system, reduced glutathione. These results clearly demonstrated the increase in oxidative stress in DOX treated rats. This condition was significantly corrected with the use of the two drugs under investigation.
Meanwhile, in this set of experiments DOX-induced cardio- and nephro-toxicity was associated with significant increase in NO level and increase in cardiac Ca2+ level. Interestingly, restoration of normal level of NO and Ca2+ was observed in DOX-rats received captopril or telmisartan in its two dose levels.
On the light of these results it is reasonable to suggest that the amelioration of DOX-induced cardio- and nephro-toxicity offered by captopril and telmisartan might be mechanistically relevant to their ability to reduce oxidative stress and to correct the distorted tissues level of NO and cardiac calcium level. However, other possible mechanisms can not be ruled out and further studies are still required to clarify this point.