Angiotensin-converting enzyme inhibition and angiotensin AT1-receptor antagonism equally improve doxorubicin-induced cardiotoxicity and nephrotoxicity

Pharmacological Research

Volumn 60, Issue 5, 2009, Pages 373-381

  Ibrahim, Mohamed A ^a   Ashour, Osama M ^a   Ibrahim, Yasmin F ^a   EL Bitar, Hussian I ^b   Gomaa, Wafaey ^a   Abdel Rahim, Salama R ^a  

^a Minia University   (Egypt)

^b Assiut University Faculty of Medicine   (Egypt)

Author keywords

Doxorubicin cardiotoxicity; Doxorubicin nephrotoxicity; Telmisartan versus captopril

Indexed keywords

ANGIOTENSIN 1 RECEPTOR; CAPTOPRIL; CREATINE KINASE MB; DIPEPTIDYL CARBOXYPEPTIDASE; DOXORUBICIN; GLUTATHIONE; GLUTATHIONE PEROXIDASE; INDUCIBLE NITRIC OXIDE SYNTHASE; LACTATE DEHYDROGENASE; MALONALDEHYDE; NITRIC OXIDE; SUPEROXIDE DISMUTASE; TELMISARTAN;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ANTIOXIDANT ACTIVITY; ARTICLE; CARDIOTOXICITY; CONTROLLED STUDY; CREATININE BLOOD LEVEL; HEART MUSCLE FIBROSIS; HEART PROTECTION; HISTOPATHOLOGY; KIDNEY TUBULE DAMAGE; LIPID PEROXIDATION; MALE; NEPHROTOXICITY; NONHUMAN; OXIDATIVE STRESS; PRIORITY JOURNAL; RAT; RENAL PROTECTION; UREA BLOOD LEVEL;

ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; ANIMALS; ANTIBIOTICS, ANTINEOPLASTIC; BENZIMIDAZOLES; BENZOATES; CAPTOPRIL; DOXORUBICIN; GLUTATHIONE; GLUTATHIONE PEROXIDASE; HEART; KIDNEY; LIPID PEROXIDATION; MALE; MYOCARDIUM; NITRIC OXIDE; NITRIC OXIDE SYNTHASE TYPE II; RATS; SUPEROXIDE DISMUTASE;

EID: 69549103071     PISSN: 10436618     EISSN: 10961186     Source Type: Journal    
DOI: 10.1016/j.phrs.2009.05.007     Document Type: Article

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