John T. Rotruck

Bio: John T. Rotruck is an academic researcher from University of Wisconsin-Madison. The author has contributed to research in topics: Glutathione & GPX6. The author has an hindex of 4, co-authored 4 publications receiving 8150 citations.

Selenium: Biochemical Role as a Component of Glutathione Peroxidase

Abstract: When hemolyzates from erythrocytes of selenium-deficient rats were incubated in vitro in the presence of ascorbate or H(2)O(2), added glutathione failed to protect the hemoglobin from oxidative damage. This occurred because the erythrocytes were practically devoid of glutathione-peroxidase activity. Extensively purified preparations of glutathione peroxidase contained a large part of the (75)Se of erythrocytes labeled in vivo. Many of the nutritional effects of selenium can be explained by its role in glutathione peroxidase.

Selenium: Biochemical Role as a Component of Glutathione Peroxidase

Abstract: When hemolyzates from erythrocytes of selenium-deficient rats were incubated in vitro in the presence of ascorbate or H(2)O(2), added glutathione failed to protect the hemoglobin from oxidative damage. This occurred because the erythrocytes were practically devoid of glutathione-peroxidase activity. Extensively purified preparations of glutathione peroxidase contained a large part of the (75)Se of erythrocytes labeled in vivo. Many of the nutritional effects of selenium can be explained by its role in glutathione peroxidase.

Glucose-dependent Protection by Dietary Selenium against Haemolysis of Rat Erythrocytes in vitro

Abstract: THE occurrence in man of drug-induced haemolysis in glucose-6-phosphate dehydrogenase (G6PD) deficient erythrocytes1 suggested the possibility of an analogy to the haemolysis which occurs in vitamin E deficient red blood cells. Cohen and Hochstein2 have shown that haemolysis in G6PD deficient cells is associated with the inability of the cell to generate adequate reduced glutathione (GSH) through GSSG reductase because of the impaired generation of NADPH. Moreover, there is evidence that glucose protects red blood cells from haemolysis by its ability to provide NADPH through G6PD which subsequently generates GSH3. The G6PD deficient cell, however, cannot maintain an adequate concentration of GSH in the cell, even in the presence of glucose4, whereas the normal cell can maintain a normal concentration of GSH in the presence of glucose, preserving the integrity of the red blood cell. Vitamin E protects red blood cells from haemolysis whether supplied in vivo or in vitro and its effect has usually been demonstrated without glucose in the incubation medium. Although selenium prevents many of the same deficiency symptoms as vitamin E, it has not been uniformly effective in preventing the in vitro haemolysis of red blood cells. If a protective action of selenium against haemolysis were dependent on the presence of GSH, or if selenium were involved in the generation of GSH, selenium would not be expected to prevent haemolysis unless glucose was present in the incubation medium to provide a constant source of NADPH for the generation of GSH from GSSG through GSSG reductase (Fig. 1).

Selenium: Biochemical Role as a Component of Glutathione Peroxidase

Abstract: When hemolyzates from erythrocytes of selenium-deficient rats were incubated in vitro in the presence of ascorbate or H(2)O(2), added glutathione failed to protect the hemoglobin from oxidative damage. This occurred because the erythrocytes were practically devoid of glutathione-peroxidase activity. Extensively purified preparations of glutathione peroxidase contained a large part of the (75)Se of erythrocytes labeled in vivo. Many of the nutritional effects of selenium can be explained by its role in glutathione peroxidase.

Trace Elements From Soil to Human

Abstract: Biogeochemistry of the Human Environment.- The Biosphere.- Soils.- Waters.- Air.- Plants.- Humans.- Biogeochemistry of Trace Elements.- Trace Elements of Group 1 (Previously Group Ia).- Trace Elements of Group 2 (Previously Group IIa).- Trace Elements of Group 3 (Previously Group IIIb).- Trace Elements of Group 4 (Previously Group IVb).- Trace Elements of Group 5 (Previously Group Vb).- Trace Elements of Group 6 (Previously Group VIb).- Trace Elements of Group 7 (Previously Group VIIb).- Trace Elements of Group 8 (Previously Part of Group VIII).- Trace Elements of Group 9 (Previously Part of Group VIII).- Trace Elements of Group 10 (Previously Part of Group VIII).- Trace Elements of Group 11 (Previously Group Ib).- Trace Elements of Group 12 (Previously Group IIb).- Trace Elements of Group 13 (Previously Group IIIa).- Trace Elements of Group 14 (Previously Group IVa).- Trace Elements of Group 15 (Previously Group Va).- Trace Elements of Group 16 (Previously Group VIa).- Trace Elements of Group 17 (Previously Group VIIa).

Organoselenium and Organotellurium Compounds: Toxicology and Pharmacology

Abstract: The organoselenium and organotellurium compounds have been described as promising pharmacological agents in view of their unique biological properties. Glutathione peroxidase mimic, antioxidant activity and thioredoxin reductase inhibition are some of the properties reviewed here. On the other hand, little is known about the molecular toxicological effects of organoselenium and organotellurium compounds. Most of our knowledge arose from research on inorganic selenium and tellurium. However, the ability to oxidize sulfhydryl groups from biological molecules can be involved both in their pharmacological properties and in their toxicological effects. In fact, exposition to high doses of organoselenium or to low doses of organotellurium causes the depletion of endogenous reduced glutathione in a variety of tissues. Thus, the design of compounds that cause low depletion of glutathione and react with specific targeted proteins, controlling specific metabolic pathways, will represent an important progress in understanding the field of organochalcogen compounds. Furthermore, the development of new organochalcogens with higher thiol-peroxidase activity that can use other non-toxic thiol reducing agents, such as N-acetylcysteine instead of glutathione, will permit the investigation of the co-administration of organochalcogens and thiols as a formulation for antioxidant therapy.