Correlation between oxidative stress and L-type calcium channel expression in the ventricular myocardia of selenium-deficient mice.

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.
CONCLUSION: L-type calcium channels were involved in selenium deficiency-induced cardiomyocyte injury, which was positively related to oxidative stress.