| Autor: |
Cui, J, Zhong, R, Chu, E, Zhang, XF, Zhang, WG, Fang, CF, Dong, Q, Li, FL, Li, H |
| Zdroj: |
Journal of International Medical Research; October 2012, Vol. 40 Issue: 5 p1677-1687, 11p |
| Abstrakt: |
Objective: Expression of the Cacna1c(calcium channel, voltage-dependent, Ltype, a1C subunit) gene was studied to investigate the relationship between oxidative stress and L-type calcium channels in the myocardium of seleniumdeficient mice.Methods: Selenium levels in liver and heart tissue samples from mice fed normal or selenium-deficientdiets were evaluated by fluorometry. In the same mice, glutathione peroxidase (GPx) and Cacna1cgene 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, GPxexpression and SOD activity were decreased, and Cacna1cexpression 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. |
| Databáze: |
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