Effect of selenium on human myocardial glutathione peroxidase gene expression.
OBJECTIVE
To examine the role of selenium (Se) in the expression and activity of selenium-dependent cellular glutathione peroxidase (GPX-1).


METHODS
46 patients with atrial septal defect or ventricular septal defect were separated into two groups, a control group (23 cases) and a Se supplementation group (23 cases). The Se supplementation group received 400 micrograms selenium per day for 7 days before surgery. We used biochemical techniques, atomic absorption, RT-PCR and cDNA sequence testing methods to evaluate and compare the changes during ischemia/reperfussion (I/R) in myocardial melondialdehyde (MDA) level, GPX activity and gene expression level, GPX cDNA nucleotide sequence, selenium and calcium and magnesium concentration.


RESULTS
Before ischemia, taking selenium for 7 days did not change the selenium concentration in either plasma or blood cells in either group. The GPX mean activity level in the selenium group was slightly lower than that in the control group, and the MDA level was equal in both. After 30 minutes of reperfusion, the Se level in plasma and blood cells remained constant, while the myocardial Se concentration and GPX gene expression in the Se group increased significantly. The MDA level in the Se group reduced 4.2%, compared to an 8.2% rise in the control group. The mean level of GPX activity in the Se group was slightly lower than that in the control group. Both pre- and post-myocardial reperfusion, the Se group had a higher rate of myocardial GPX gene expression, and the nucleotide sequence was normal. These results indicate that supplementing Se is not likely to enhance myocardial GPX activity, but it could increase the GPX gene expression level, and thereby enhance the Se patients' myocardial antioxidant level during I/R, allowing free radicals to be scavenged as soon as they are generated.


CONCLUSIONS
Se supplementation could increase myocardial selenium content and improve GPX gene expression during I/R, and in this way defend against free radical peroxide damage to the myocardium.
Liu
D
D
Beijing Institute of Heart Lung & Blood Vessel Diseases, Beijing 100029, China.
Liu
S
S
Huang
Y
Y
Liu
Y
Y
Zhang
Z
Z
Han
L
L
D000293:Adolescent; D000328:Adult; D001483:Base Sequence; D002648:Child; D018076:DNA, Complementary / Q000737:chemistry / Q000235:genetics; D005260:Female; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D005979:Glutathione Peroxidase / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008969:Molecular Sequence Data; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism*; D012333:RNA, Messenger / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D012643:Selenium / Q000097:blood / Q000378:metabolism / Q000494:pharmacology*; D016415:Sequence Alignment; D017422:Sequence Analysis, DNA; D012689:Sequence Homology, Nucleic Acid
D018076:DNA, Complementary; D012333:RNA, Messenger; D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D012643:Selenium