Effect of sodium selenosulfate on restoring activities of selenium-dependent enzymes and selenium retention compared with sodium selenite in vitro and in vivo.
Sodium selenosulfate has been extensively used as a precursor of selenide ions in the preparation of nano Se-containing compounds. Its biological properties remain completely unknown. Sodium selenosulfate and sodium selenite were added to the medium of HepG2 cells and administered intraperitoneally at a dose of 0.1 mg Se/kg body weight to selenium-deficient mice, respectively. Both of the selenium compounds could increase the activities of glutathione peroxidase (GPx) and thioredoxin reductase (TrxR) in a dose-dependent manner in cells and efficiently restore selenium retention and activities of GPx and TrxR in mice. All of the variables were in correlation with the Se supply. There was no distinction in elevating activities of GPx and TrxR between selenosulfate and selenite in vitro. After a 2-d supply of selenosulfate, the activity of GPx in the liver was 65% (p<0.001) and Se accumulations in the liver, kidney and blood were 64%, 86%, and 65%, respectively, of those treated with selenite (all p<0.01). With the 7-d selenosulfate supplementation, the activity of GPx in the kidney and activities of TrxR in the liver and kidney were 88%, 75%, and 78%, respectively, of those treated with selenite (all p<0.01); Se retentions in the liver and kidney were 85% and 93%, respectively of those supplemented with selenite (both p<0.01). These facts indicated that selenosulfate could be absorbed and utilized in the biological system. No difference in vitro demonstrated that selenosulfate could be absorbed and generate reduced selenide as efficiently as selenite. The differences between the two compounds in vivo were the result of other factors that affected selenosulfate utilization in tissues.
Peng
Dungeng
D
University of Science and Technology of China, Heifi, Anhui, 230052, People's Republic of China.
Zhang
Jinsong
J
Liu
Qinliang
Q
D000818:Animals; D045744:Cell Line, Tumor; D005979:Glutathione Peroxidase / Q000378:metabolism*; D006801:Humans; D008297:Male; D051379:Mice; D012643:Selenium / Q000737:chemistry* / Q000172:deficiency / Q000502:physiology*; D018036:Selenium Compounds / Q000494:pharmacology*; D018038:Sodium Selenite / Q000494:pharmacology*; D013431:Sulfates / Q000494:pharmacology*; D013880:Thioredoxin-Disulfide Reductase / Q000378:metabolism*
D018036:Selenium Compounds; D013431:Sulfates; D005979:Glutathione Peroxidase; C080439:selenium-independent glutathione peroxidase; D013880:Thioredoxin-Disulfide Reductase; D012643:Selenium; D018038:Sodium Selenite; C519925:sodium selenosulfate