Effect of sodium selenosulfate on restoring activities of selenium-dependent enzymes and selenium retention compared with sodium selenite in vitro and in vivo

Abstract

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.

Biogenic selenium and its hepatoprotective activity

“…One hundred Se-deficient mice were randomly divided into the following ten groups with 10 mice per group (in accordance to Table 3 ). The doses of Se were chosen according to the report by Peng 50 . Mice were fed a Se-deficient diet (<0.02 μg Se/g diet) during the experimental phase of the study.…”

Anti‐cancer potential of selenium‐ and tellurium‐containing species: opportunities abound!

“…A different form of selenium with significantly lower toxicity would make selenium modulation of cisplatin toxicity more practicable. A candidate has been identified in selenosulfate ( − SeS(═O) 2 O − , 7 ) which equally, with 6 , elevates the activity of glutathione peroxidase and thioredoxin reductase in the human liver hepatocellular carcinoma cell line, HepG2 . Conversely, the bioavailability of 7 in terms of increasing selenium accumulation and the formation of selenoenzymes was marginally but significantly less than that mediated by 6 in selenium‐deficient mice at nutritional doses .…”

“…A candidate has been identified in selenosulfate ( − SeS(═O) 2 O − , 7 ) which equally, with 6 , elevates the activity of glutathione peroxidase and thioredoxin reductase in the human liver hepatocellular carcinoma cell line, HepG2 . Conversely, the bioavailability of 7 in terms of increasing selenium accumulation and the formation of selenoenzymes was marginally but significantly less than that mediated by 6 in selenium‐deficient mice at nutritional doses . The utilization of 7 as the source of selenium within the dose range required for the moderation of cisplatin toxicity is the same as that of 6 , an important finding as 7 is significantly less toxic than 6 .…”

MS07116 Sodium Selenosulfate Synthesis and Demonstration of Its In Vitro Cytotoxic Activity Against HepG2, Caco2, and Three Kinds of Leukemia Cells

“…As to the biological effects of sodium selenosulfate, we previously reported that sodium selenosulfate increased the activity of glutathione peroxidase and thioredoxin reductase in HepG2 cells; however, the bioavailability of selenosulfate in terms of increasing selenoenzymes and selenium accumulation was slightly but significantly less than selenite in selenium-deficient mice at a nutritional dose [11]. In the present study, we describe its cytotoxic effect against HepG2, Caco2, and three kinds of leukemia cells.…”