title: Preventive effects of selenium yeast, chromium picolinate, zinc sulfate and their combination on oxidative stress, inflammation, impaired angiogenesis and atherogenesis in myocardial infarction in rats.
abstract: OBJECTIVE
  Accumulating evidences suggest a critical role of trace metal dyshemostasis in oxidative stress and cardiac dysfunction after myocardial infarction (MI). This study investigated the cardioprotective effects of selenium yeast (Se), chromium picolinate Cr(pic)3, zinc sulfate (Zn) and their combination on isoproterenol (ISO)-induced MI.
  
  
  METHODS
  Rats were divided into six groups: normal control, ISO control, Se-pretreated (0.1 mg/kg), Cr(pic)3-pretreated (400 µg/kg), Zn-pretreated (30 mg/kg) and metal combination-pretreated groups. All metals were administered for 28 days and at the 27th day, MI was induced by subcutaneous injection of ISO (85 mg/kg) once for two consecutive days.
  
  
  RESULTS
  ISO control group showed hyperlipidemia, elevation of cardiac biomarkers and lipid peroxidation and increased immunostaining of p47 phox NADPH oxidase subunit in addition to decreased levels of glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx). Cardiac levels of tumor necrosis factor-α (TNF-α) were increased, while vascular endothelial growth factor (VEGF, the major angiogenic factor) was decreased. Pretreatment with Se normalized the cardiac enzymes, lipid peroxidation, GSH, SOD, CAT, GPx, TNF-α and VEGF (P<0.001) and reduced the immunostaining of p47 phox subunit. However, Se failed to correct the dyslipidemia. Cr(pic)3 significantly improved lipid profile (P<0.001) and all other biochemical deviations except for VEGF. Zn, but to lesser extent, reduced the oxidative damage and TNF-α levels and improved both dyslipidemia and angiogenesis. Combination therapy exhibited less prominent protection compared to individual metals.
  
  
  CONCLUSIONS
  Daily supplementation with trace metals is promising for improving myocardial performance via preventing oxidative damage, induction of angiogenesis, anti-inflammatory and/or anti-hyperlipidemic mechanisms.
authors.affiliation: King Saud University.
authors.forename: Nouf M
authors.initials: NM
authors.lastname: Al-Rasheed
authors.forename: Hala A
authors.initials: HA
authors.lastname: Attia
authors.forename: Raessa A
authors.initials: RA
authors.lastname: Mohamed
authors.forename: Nawal M
authors.initials: NM
authors.lastname: Al-Rasheed
authors.forename: Maha A
authors.initials: MA
authors.lastname: Al-Amin
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000517:prevention & control; D002316:Cardiotonic Agents / Q000097:blood / Q000493:pharmacokinetics / Q000627:therapeutic use*; D004359:Drug Therapy, Combination; D050171:Dyslipidemias / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D007249:Inflammation / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D007545:Isoproterenol; D008297:Male; D009203:Myocardial Infarction / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D019255:NADPH Oxidases / Q000378:metabolism; D018919:Neovascularization, Physiologic / Q000502:physiology; D018384:Oxidative Stress / Q000187:drug effects; D010848:Picolinic Acids / Q000097:blood / Q000493:pharmacokinetics / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D012441:Saccharomyces cerevisiae; D012643:Selenium / Q000097:blood / Q000493:pharmacokinetics / Q000627:therapeutic use*; D019287:Zinc Sulfate / Q000097:blood / Q000493:pharmacokinetics / Q000627:therapeutic use*
chemical_list: D002316:Cardiotonic Agents; D010848:Picolinic Acids; D019287:Zinc Sulfate; D019255:NADPH Oxidases; C060505:neutrophil cytosolic factor 1; D012643:Selenium; D007545:Isoproterenol; C030614:picolinic acid