The antioxidant role of selenium and seleno-compounds

doi:10.1016/S0753-3322(03)00035-0

Biomedicine & Pharmacotherapy

Volume 57, Issues 3–4, May 2003, Pages 134-144

https://doi.org/10.1016/S0753-3322(03)00035-0 Get rights and content

Abstract

Selenium (Se) is an essential trace element for animals and humans that is obtained from dietary sources including cereals, grains and vegetables. The Se content of plants varies considerably according to its concentration in soil. Plants convert Se mainly into Se-methionine (Se-Met) and incorporate it into protein in place of methionine (Met). Selenocystine (Se-Cys), methyl-Se-Cys and γ-glutamyl-Se-methyl-Cys are not significantly incorporated into plant protein and are at relatively low levels irrespective of soil Se content. Higher animals are unable to synthesize Se-Met and only Se-Cys was detected in rats supplemented with Se as selenite. Renal regulation is the mode by which whole body Se is controlled. Se is concentrated in hair and nail and it occurs almost exclusively in organic compounds. The potentiating effect of Se deficiency on lipid peroxidation is enhanced in some tissues by concurrent deficiency of copper or manganese. In the in vitro system, the chemical form of Se is an important factor in eliciting cellular responses. Although the cytotoxic mechanisms of selenite and other redoxing Se compounds are still unclear, it has been suggested that they derive from their ability to catalyze the oxidation of thiols and to produce superoxide simultaneously. Selenite-induced cytotoxicity and apoptosis in human carcinoma cells can be inhibited with copper (CuSO₄) as an antioxidant. High doses of selenite result in induction of 8-hydroxydeoxyguanosine (8-OHdG) in mouse skin cell DNA and in primary human keratinocytes. It may cause DNA fragmentation and decreased DNA synthesis, cell growth inhibition, DNA synthesis, blockade of the cell cycle at the S/G₂-M phase and cell death by necrosis. In contrast, in cells treated with methylselenocyanate or Se methylselenocysteine, the cell cycle progression was blocked at the G₁ phase and cell death was predominantly induced by apoptosis.

Section snippets

Bioavailability and distribution

The selenium (Se) content of plants varies tremendously according to its concentration in soil which varies regionally. Volcanic soils are particularly susceptible to mineral leaching. Around the world, there are the regions that are so Se poor that overt deficiency syndromes are endemic: these regions include arid regions of Australia, northeast China, northern North Korea, south central China, Nepal and Tibet. Central Africa, particularly the Democratic Republic of Congo has similar

Pathologies associated with Se deficiency

Se deficiency affects glutathione (GSH) metabolism by increasing its synthesis and release in the liver with concomitant increase in plasma GSH [10]. Increased plasma GSH can lead to a depletion of cysteine and impairment of protein synthesis. Se deficiency is also accompanied by a decrease in glutathione peroxidase (GSH-Px) activity and results in an increase in hepatic glutathione-S-transferase (GST) activity [11]. Recently, it has been reported that Se deficiency decreases the plasma

The selenoproteins

All mammalian selenoproteins contain Se in the form of the amino acid selenocysteine (Sec) which is encoded by the UGA triplet. There are two forms of tRNA^[Ser]Sec, which are essential for the synthesis of all selenoproteins. The tRNA^[Ser]Sec isoforms are both the site of Sec synthesis and the adaptor molecules which recognize the appropriate UGA codons in selenoprotein mRNAs. Twenty-two known eukaryotic selenoproteins are organized into distinct selenoprotein groups on the basis of the

Se in cancer prevention

A confluence of evidences show an association between Se and the processes which lead to, or prevent, cancers [75], [76], [77], [78], [79]. In animal models, supplementation of inorganic Se in the diet protects against cancer induced by a variety of chemical carcinogens [80]. Se compounds like selenite and selenate have strong inhibitory effects particularly on mammalian tumor cell growth. The mechanism of action of selenite and selenate appears to be distinct. Cells treated with selenite

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Cadmium tellurium quantum dots (CdTe QDs) as one of the most widely used QDs have been reported the toxicity and biosafety in recent years, little work has been done to reduce their toxicity however. Based on the mechanisms of toxicity of CdTe QDs on liver target organs such as oxidative stress and apoptosis previously reported by other researchers, we investigated the mechanism of action of trace element selenium (Se) to mitigate the hepatotoxicity of CdTe QDs. The experimental results showed that Se-Met at 40–140 μg L⁻¹ could enhance the function of intracellular antioxidant defense system and the molecular structure of related antioxidant enzymes by reduce the production of ROS by 45%, protecting the activity of antioxidants and up-regulating the expression of selenoproteins with antioxidant functions, Gpx1 increase 225% and Gpx4 upregulated 47%. In addition, Se-Met could alleviate CdTe QDs-induced apoptosis by regulating two apoptosis-inducing factors, as intracellular caspase 3/9 expression levels were reduced by 70% and 87%, decreased Ca²⁺ concentration, and increased mitochondrial membrane potential measurements. Overall, this study indicates that Se-Met has a significant protective effect on the hepatotoxicity of CdTe QDs. Se-Met can be applied to the preparation of CdTe QDs to inhibit its toxicity and break the application limitation.
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Dossier: Oxidative stress pathologies and antioxidantsThe antioxidant role of selenium and seleno-compounds

Abstract

Section snippets

Bioavailability and distribution

Pathologies associated with Se deficiency

The selenoproteins

Se in cancer prevention

J Nutr

Am J Clin Nutr

J Nutr

J Nutr

Biomed Pharmacother

Biomed Pharmacother

Biomed Pharmacother

Biomed Pharmacother

J Nutr

Am J Clin Nutr

Am J Clin Nutr

Lancet

Free Radic Biol M

J Biol Chem

Arch Biochem Biophys

Biochim Biophys Acta

J Nutr

J Biol Chem

J Nutr

J Trace Elem Med Biol

Biochim Biophys Acta

Am J Pathol

J Biol Chem

J Nutr

Hepatology

J Biol Chem

J Biol Chem

Biochem Pharmacol

Exp Cell Res

Biochem Biophys Res Commun

J Biol Chem

J Nutr

J Nutr

Pharmacol Ther

Lancet

Am J Clin Nutr

Uptake of selenite, selenomethionine and selenate by brush border membrane vesicles isolated from rat small intestine

Biometals

The assessment of bioavailability of micronutrients: introduction

Eur J Clin Nutr

Effect of dietary methionine on tissue selenium and glutathione peroxidase on tissue selenium and glutathione peroxidase activity given selenomethionine

Br J Nutr

Bioavailability of selenium

Eur J Clin Nutr

Selenium speciation in human milk with special respect to quality control

Biol Trace Elem Res

Pathways of selenium metabolism including respiratory excretory products

J Am Coll Toxicol

Selenium in the central nervous system of rats exposed to 75-Se selenomethionine and sodium selenite

Biol Trace Elem Res

Liver and kidney necrosis in selenium deficient rats depleted of glutathione

Lab Invest

Nutritional regulation of homocysteine: effects of drugs

Biomed Pharmacother

Rapid genomic evolution of a non-virulent Coxsackie virus B3 in selenium deficient mice results in selection of identical isolates

Nature M

The effect of selenium-fortified table salt in the prevention of Keshan disease on a population of 1.05 million

Biomed Environ Sci

Factors affecting the selenium intake of people in transbaikalian Russia

Biol Trace Element Res

Pathologic anatomy of the dilated cardiomyopathies

Am J Cardiol

Dossier: Oxidative stress pathologies and antioxidants
The antioxidant role of selenium and seleno-compounds