title: Correlation between oxidative stress and L-type calcium channel expression in the ventricular myocardia of selenium-deficient mice.
abstract: OBJECTIVE
  Expression of the Cacna1c (calcium channel, voltage-dependent, L-type, α1C subunit) gene was studied to investigate the relationship between oxidative stress and L-type calcium channels in the myocardium of selenium-deficient mice.
  
  
  METHODS
  Selenium levels in  liver and heart tissue samples from mice fed normal or selenium-deficient diets were evaluated by fluorometry. In the same mice, glutathione peroxidase (GPx) and Cacna1c gene expression were analysed, malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were  measured, oxidoreductase gene expression profiles were analysed (by DNA microarray), and myocardial structural changes were studied.
  
  
  RESULTS
  In selenium-deficient versus control mice, GPx expression and SOD activity were decreased, and Cacna1c expression and MDA concentration  were increased. Selenoprotein oxidoreductase and nonselenoprotein oxidoreductase gene expression differed significantly between selenium-deficient and control mice. In selenium-deficient mice, myocardial fibres were separated by loose collagenous tissue; electron microscopy showed shortened  sarcomeres, dilated sarcoplasmic reticulum, scattered myofibril lysis and increased mitochondria with amorphous matrix densities.
  
  
  CONCLUSIONS
  L-type calcium channels were involved in selenium deficiency-induced cardiomyocyte injury, which was positively related to oxidative stress.
authors.affiliation: Harbin Medical University, Harbin, Hei Longjiang Province, China.
authors.forename: J
authors.initials: J
authors.lastname: Cui
authors.forename: R
authors.initials: R
authors.lastname: Zhong
authors.forename: E
authors.initials: E
authors.lastname: Chu
authors.forename: X F
authors.initials: XF
authors.lastname: Zhang
authors.forename: W G
authors.initials: WG
authors.lastname: Zhang
authors.forename: C F
authors.initials: CF
authors.lastname: Fang
authors.forename: Q
authors.initials: Q
authors.lastname: Dong
authors.forename: F L
authors.initials: FL
authors.lastname: Li
authors.forename: H
authors.initials: H
authors.lastname: Li
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism; D020746:Calcium Channels, L-Type / Q000235:genetics / Q000378:metabolism*; D004032:Diet; D005260:Female; D015870:Gene Expression; D006352:Heart Ventricles / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D020411:Oligonucleotide Array Sequence Analysis; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism; D012643:Selenium / Q000172:deficiency*; D051140:Selenoproteins / Q000235:genetics / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D059467:Transcriptome
chemical_list: C514350:CACNA1C protein, mouse; D020746:Calcium Channels, L-Type; D017382:Reactive Oxygen Species; D051140:Selenoproteins; D013482:Superoxide Dismutase; D012643:Selenium