Selenium supplementation prevents the increase in atherogenic electronegative LDL (LDL minus) in the postprandial phase.
Evidence is accumulating that postprandial phenomena play a role in atherogenesis. Dietary lipid hydroperoxides that escape from the gastrointestinal barrier can be incorporated into plasma lipoproteins, leading to a modified form of LDL (LDL minus). The present human study was designed to investigate the effect of selenium supplementation on the formation of LDL minus in the postprandial phase. Fourteen healthy subjects ate the same test meal, high in lipid hydroperoxides, at baseline and after 10-day selenium supplementation (110 microg/day). Plasma selenium, LDL minus, LDL resistance to oxidative modification, plasma antioxidants (ascorbic acid, GSH and GPx activity) and MDA were measured in preprandial (time 0) and postprandial (3h) phases. Supplementation did not induce changes in the concentration of selenium in fasting plasma, but, at the same time, it induced a significant decrease in preprandial plasma GPx activity and inhibited the meal-induced increase in GPx activity. Selenium supplementation fully prevented the meal-induced increase in both LDL minus level and LDL susceptibility to oxidation. This study demonstrated the efficacy of selenium in preventing postprandial oxidative stress. The results, obtained on subjects adequately supplied with selenium, suggest that a non-limiting selenium availability counteracts the postprandial formation of the atherogenic form of LDL and provide a rationale for the epidemiological evidence of the inverse correlation between selenium intake and the incidence of chronic and degenerative diseases.
Natella
Fausta
F
Free Radical Research Group, National Research Institute for Food and Nutrition, Via Ardeatina 546, 00178 Roma, Italy. natella@inran.it
Fidale
Michela
M
Tubaro
Franco
F
Ursini
Fulvio
F
Scaccini
Cristina
C
D000328:Adult; D000975:Antioxidants / Q000378:metabolism*; D001205:Ascorbic Acid / Q000097:blood; D019587:Dietary Supplements; D005260:Female; D005978:Glutathione / Q000097:blood / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000097:blood; D006801:Humans; D015227:Lipid Peroxidation / Q000187:drug effects*; D008054:Lipid Peroxides / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood*; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects*; D019518:Postprandial Period / Q000187:drug effects / Q000502:physiology; D012643:Selenium / Q000008:administration & dosage / Q000494:pharmacology*
D000975:Antioxidants; D008054:Lipid Peroxides; D008077:Lipoproteins, LDL; D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D005978:Glutathione; D012643:Selenium; D001205:Ascorbic Acid