title: Hexavalent chromium inhibited the expression of RKIP of heart in vivo and in vitro.
abstract: BACKGROUND
  Chromium (Cr) is considered to be a risk factor to the cardiovascular effects of fine particulate matter components to PM2.5 from traffic in highway patrol officers. RKIP (raf kinase inhibitor protein) is a physiological inhibitor of GRK-2 (G-protein-coupled receptor kinase 2) and affects β-adrenergic signaling and contractile activity in cardiomyocytes.
  
  
  OBJECTIVE
  In this study, we explored the change of RKIP in heart of chromium (VI)-exposed rats and cultured myocardial cells with chromium (VI) treatment.
  
  
  METHODS
  Wistar rats were divided into six groups which were chronically fed with 250, 500, 750, 1000, and 1250 ppm Na(2)Cr(2)O(7) and water for 60 days, respectively. Na(2)Cr(2)O(7) dose of 0.25, 0.5, 1.5, 3, 4.5, and 0 ppm (control group) was applied in cultured myocardial cells. The level of heart Cr (VI) was determined by electrothermal atomic absorption spectrometry. The expression of RKIP was measured by Western blot method. The MTT assay was used to measure the toxicity of myocardial cells with Cr (VI) treatment. The apoptosis test of myocardial cells was determined by caspase-3 colorimetric assay kit.
  
  
  RESULTS
  The result showed that the expression of RKIP in heart (in vivo) and myocardial cells (in vitro) was decreased following Cr (VI) dose-dependent treatment.
  
  
  CONCLUSIONS
  We suggested that the decrement of RKIP of heart and myocardial cells with Cr (VI) treatment resulted in the function of cardiovascular system decreased.
authors.affiliation: Department of Biomedical Engineering, I-Shou University, Dashu Shiang, Kaohsiung County, Taiwan. huoy@isu.edu.tw
authors.forename: Huoy-Rou
authors.initials: HR
authors.lastname: Chang
authors.forename: Der-An
authors.initials: DA
authors.lastname: Tsao
authors.forename: Wei-Chang
authors.initials: WC
authors.lastname: Tseng
mesh_terms: D000393:Air Pollutants / Q000493:pharmacokinetics / Q000633:toxicity*; D000818:Animals; D000831:Animals, Newborn; D017209:Apoptosis / Q000187:drug effects; D053148:Caspase 3 / Q000378:metabolism; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D002840:Chromates / Q000008:administration & dosage / Q000493:pharmacokinetics / Q000633:toxicity; D002857:Chromium / Q000032:analysis; D017608:Chromium Compounds / Q000008:administration & dosage / Q000493:pharmacokinetics / Q000633:toxicity*; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation / Q000187:drug effects*; D006321:Heart / Q000187:drug effects* / Q000254:growth & development; D008297:Male; D009206:Myocardium / Q000737:chemistry / Q000166:cytology / Q000378:metabolism*; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism; D052638:Particulate Matter / Q000633:toxicity; D051381:Rats; D017208:Rats, Wistar; D014018:Tissue Distribution
chemical_list: D000393:Air Pollutants; D002840:Chromates; D017608:Chromium Compounds; D052638:Particulate Matter; D002857:Chromium; C016104:sodium bichromate; C505410:Casp3 protein, rat; D053148:Caspase 3