title: Protective effect of telmisartan against cadmium-induced nephrotoxicity in mice.
abstract: OBJECTIVE
  To investigate the nephroprotective effect of telmisartan, the angiotensin II receptor antagonist, against renal injury induced by cadmium in mice.
  
  
  METHODS
  Mice received cadmium chloride at a dose of 1.2mg Cd/kg/day, s.c., for nine weeks. Telmisartan treatment (1mg/kg/day, orally) was started one week before cadmium administration and continued for ten weeks.
  
  
  RESULTS
  Telmisartan significantly reduced blood urea nitrogen (BUN) and serum creatinine levels which were increased by cadmium. Also, telmisartan significantly suppressed lipid peroxidation, compensated deficits in the antioxidant defenses [reduced glutathione (GSH) level and catalase activity], decreased the elevations of tumor necrosis factor-α (TNF-α), nitric oxide (NO) and cadmium ion concentration, and attenuated the reductions of selenium and zinc ions in renal tissue resulted from cadmium administration. Histopathological examination revealed that cadmium-induced renal tissue damage was ameliorated by telmisartan treatment. Immunohistochemical analysis revealed that telmisartan significantly decreased the cadmium-induced overexpression of inducible nitric oxide synthase (iNOS), nuclear factor-κB (NF-κB), Fas ligand (FasL) and caspase-3 in renal tissue.
  
  
  CONCLUSIONS
  Telmisartan, through its antioxidant and anti-inflammatory actions, effectively prevented cadmium nephrotoxicity in mice. Hence, telmisartan represents a potential candidate to protect the kidney from the detrimental effect of cadmium toxicity.
authors.affiliation: Department of Biomedical Sciences, Pharmacology Division, College of Medicine, King Faisal University, Al-Ahsa, Saudi Arabia. amrfouad65@yahoo.com
authors.forename: Amr A
authors.initials: AA
authors.lastname: Fouad
authors.forename: Iyad
authors.initials: I
authors.lastname: Jresat
mesh_terms: D057911:Angiotensin Receptor Antagonists / Q000494:pharmacology*; D000818:Animals; D001562:Benzimidazoles / Q000494:pharmacology*; D001565:Benzoates / Q000494:pharmacology*; D001806:Blood Urea Nitrogen; D002104:Cadmium / Q000378:metabolism / Q000633:toxicity*; D002374:Catalase / Q000097:blood; D003401:Creatine / Q000097:blood; D053222:Fas Ligand Protein / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects*; D005978:Glutathione / Q000097:blood; D007150:Immunohistochemistry; D007668:Kidney / Q000187:drug effects*; D007674:Kidney Diseases / Q000139:chemically induced / Q000517:prevention & control*; D015227:Lipid Peroxidation / Q000187:drug effects; D051379:Mice; D016328:NF-kappa B / Q000378:metabolism; D009569:Nitric Oxide / Q000097:blood; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D000077333:Telmisartan; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D057911:Angiotensin Receptor Antagonists; D001562:Benzimidazoles; D001565:Benzoates; D053222:Fas Ligand Protein; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D002104:Cadmium; D009569:Nitric Oxide; D002374:Catalase; D052247:Nitric Oxide Synthase Type II; D005978:Glutathione; D003401:Creatine; D000077333:Telmisartan