Effects of selenium and tellurium on the activity of selenoenzymes glutathione peroxidase and type I iodothyronine deiodinase, trace element thyroid level, and thyroid hormone status in rats.

Tellurium (Te) and selenium (Se) belong chemically to the VIa group of elements. Se represents an essential element closely related to thyroid function. Te has growing application in industrial processes. Little is known about the Te biological activity, particularly with respect to potential chemical interactions with Se-containing components in the organism. In this study, female Wistar rats (body weight: 115-120 g) received sodium selenite pentahydrate (10 mg/L) or sodium tellurite (9.4 mg/L) in drinking water for 6 wk. Additional groups of rats received their combination with zinc sulfate heptahydrate (515 mg/L). The stimulation of 5'-DI-I activity due to selenite (to 158%, p<0.01) or tellurite treatment (to 197%, p<0.01) was seen; however, no effect on glutathione peroxidase was demonstrated in this experiment. An elevation of T4, T3, and rT3 serum levels was measured in the Se+Te-treated group; T4 and rT3 levels were elevated in the Te+Zn-treated group. Te accumulates in the thyroid gland and influences the zinc thyroid level. Te treatment alone and in combination with Se or Zn decreased the iodine thyroid concentration to 65-70% of the control value. Further studies are needed to clarify the nature and effects of these events.

Role of copper, zinc, selenium and tellurium in the cellular defense against oxidative and nitrosative stress.

The trace elements copper, zinc and selenium are linked together in cytosolic defense against reactive oxygen and nitrogen species. Copper, zinc-superoxide dismutase catalyzes the dismutation of superoxide to oxygen and hydrogen peroxide. The latter and other hydroperoxides are subsequently reduced by the selenoenzyme glutathione peroxidase (GPx). Cytosolic GPx can also act as a peroxynitrite reductase. The antioxidative functions of these trace elements are not confined to being constituents of enzymes: 1) copper and zinc ions may stimulate protective cellular stress-signaling pathways such as the antiapoptotic phosphoinositide-3-kinase/Akt cascade and may stabilize proteins, thereby rendering them less prone to oxidation; and 2) selenium does not only exist in the cell as selenocysteine (as in GPx) but also as selenomethionine, which is regularly present in low amounts in proteins in place of methionine. Selenomethionine catalyzes the reduction of peroxynitrite at the expense of glutathione. Also, low-molecular-weight organoselenium and organotellurium compounds of pharmacologic interest catalyze the reduction of hydroperoxides or peroxynitrite with various cellular reducing equivalents.

Biochemistry of tellurium.

Tellurium (Te) demonstrates properties similar to those of elements known to be toxic to humans, and has applications in industrial processes, which are rapidly growing in importance and scale. It is relevant, therefore, to consider the tellurium physiology, toxicity, and methods for monitoring the element in biological and environmental specimens. Animal studies suggest that up to 25% of orally administered tellurium is absorbed in the gut. There is a biphasic elimination from the circulation with loss of about 50% within a short period, t1/2 = 0.81 d, and slower elimination of the residual Te, t1/2 = 12.9 d. Following a single ip, injection the largest proportion is in the kidney and bone, but with repeated oral administration, Te is found in the heart > > kidney, spleen, bone, and lung. Formation of dimethyl telluride is a characteristic feature of exposure, and gives a pungent garlic-like odor to breath, excreta, and the viscera. The main target sites for Te toxicity are the kidney, nervous system, skin, and the fetus (hydrocephalus). Te can be reliable measured in different specimens by several analytical techniques. Recent work has employed hydride generation atomic absorption spectrometry. Topics for further investigation are proposed.