Metabolic and functional defects in selenium deficiency

This paper is concerned with present-day knowledge of the biological role of selenium, of its interaction with other nutrients including trace elements, and with the importance of selenium in human nutrition and health. Selenium has been shown to be an integral part of glutathione peroxidase, which catalyses the reduction of a large range of lipid hydroperoxides and hydrogen peroxide. The interrelation between vitamin E, selenium and polyunsaturated fatty acids is complex. First, selenium in glutathione peroxidase may control intracellular levels of hydrogen peroxide, which affect the formation of active oxygen metabolites that may serve as initiators of lipid peroxidation; this role of selenium is closely related to that of superoxide dismutases, which control intracellular levels of the superoxide anion. Secondly, vitamin E may control the formation of lipid hydroperoxides through its antioxidant function, as well as possibly entering into a structural relation with membrane phospholipids. Thirdly, glutathione peroxidase may catalyse the reduction of lipid hydroperoxides, formed from membrane lipids, to hydroxyacids without detriment to the cellular economy. In the field of human nutrition, the lack of selenium has been shown to be the cause of a cardiomyopathy known as Keshan disease, occurring in the People’s Republic of China. Blood selenium levels in patients from this area are compared with blood selenium levels in three other parts of the world and the conclusion is reached that the blood selenium level of populations in Keshan disease regions are exceptionally low and that Keshan disease is the first demonstration that selenium is an essential trace element for man.

1987 ◽  
Vol 242 (2) ◽  
pp. 383-386 ◽  
Author(s):  
C G Fraga ◽  
R F Arias ◽  
S F Llesuy ◽  
O R Koch ◽  
A Boveris

The role of vitamin E and selenium as protective agents against oxidative stress was evaluated by measuring liver chemiluminescence in situ. Weanling rats fed a vitamin E- and selenium-deficient diet showed liver chemiluminescence that was increased 60 and 100% over control values at 16 and 18 days respectively after weaning. At day 21, the double deficiency led to hepatic necrosis, as observed by optical and electron microscopy, and increased serum levels of lactate dehydrogenase and alanine aminotransferase. Single deficiencies, in either vitamin E or selenium, did not produce liver necrosis but increased liver chemiluminescence. Vitamin E deficiency led to a 23 and 50% increase in liver emission at days 18 and 20 respectively; selenium deficiency produced a 64% increase at day 16. The activity of liver selenium-glutathione peroxidase diminished to 13% of the control value in the rats fed doubly deficient and selenium-deficient diets. Activities of superoxide dismutase, catalase and non-selenium-glutathione peroxidase were not modified by the different diets. These results suggest that oxy-radical generation may play a major role in hepatic necrosis in vitamin E- and selenium-deficiency.


Author(s):  
Csaba Attila Kósa ◽  
Krisztina Nagy ◽  
Ottó Szenci ◽  
Boglárka Baska-Vincze ◽  
Emese Andrásofszky ◽  
...  

Abstract A severe form of recurrent exertional rhabdomyolysis occurs enzootically in a well-defined region of Transylvania, Harghita county. At the highest lying two settlements (more than 800 m above sea level), the prevalence of equine rhabdomyolysis is between 17 and 23%, while in the neighbouring villages in the valley it is less than 2%. The objective of our study was to clarify the role of selenium and vitamin E in the high prevalence of rhabdomyolysis in that region. Soil and hay samples were collected from each area to evaluate mineral content. Ten horses from the non-affected and 20 horses from the affected area were tested for serum selenium, vitamin E, glutathione peroxidase (GSH-Px), muscle enzymes, lactate and electrolytes. Hay samples collected from the affected area had lower selenium content. Horses in the affected regions had significantly lower serum selenium (P = 0.006) and GSH-Px levels than animals living in the non-affected regions. A good correlation between erythrocyte GSH-Px and serum selenium concentration could be demonstrated (r = 0.777, P < 0.001). Serum vitamin E levels were low independently of the origin of the horse. Based on our results, selenium deficiency possibly has a role in the Transylvanian enzootic equine recurrent rhabdomyolysis syndrome.


2018 ◽  
Vol 374 (1) ◽  
pp. 111-120 ◽  
Author(s):  
Fazal Ur Rehman Bhatti ◽  
Song Ja Kim ◽  
Ae-Kyung Yi ◽  
Karen A. Hasty ◽  
Hongsik Cho

1986 ◽  
Vol 55 (2) ◽  
pp. 305-311 ◽  
Author(s):  
J. G. Bell ◽  
B. J. S. Pirie ◽  
J. W. Adron ◽  
C. B. Cowey

1. Two duplicate groups of rainbow trout (Sulmo gairdneri; mean weight 27 g) were given diets of differing selenium content (deficient 0, 025 mg Se/kg; supplemented 1.022 mg Se/kg) for 30 weeks.2. There were no significant differences between treatments in weight gain but packed cell volume, liver vitamin E and liver and plasma Se concentrations were all significantly lower in the Se-deficient trout.3. Ataxia occurred in about 10% of the Se-deficient trout and histopathologies were evident in nerve cord (damage to axon sheath) and liver (loss of integrity in endoplasmic reticulum and mitochondria with appearance of increased vesiculation).4. Glutathione peroxidase (EC 1.11.1.9) activity was significantly reduced in liver and plasma of Se-deficient fish but there was no indication, from differential assay, of any non-Se-dependent glutathione peroxidase activity. Glutathione transferase (EC 2.5. I.18) activity was significantly increased in Se-deficient trout.


1983 ◽  
Vol 7 ◽  
pp. 128-128
Author(s):  
J. R. Arthur ◽  
R. Boyne

Deficiencies of selenium (Se) and vitamin E can result in myopathies in cattle and sheep but the mechanics have not been clearly described. Both Se, as a component of the enzyme glutathione peroxidase, and vitamin E as a radicle scavenger, are involved in the protection of cells against the toxic effects of oxygen. In young calves, Se/vitamin E deficiency can result in the death of the animals due to a focal myopathy occurring in heart muscle; focal lesions are also found in skeletal muscle. In older calves, a more diffuse myopathy is usually confined to skeletal muscle and usually occurs when cattle are turned out from winter housing to spring pasture. However, low Se/vitamin E status will not invariably result in clinical symptoms of myopathy and other factors may be involved. This report describes some of the biochemical changes which can occur during the onset of clinical myopathy in Se/vitamin E-deficient cattle.


2016 ◽  
Vol 94 (4) ◽  
pp. 305-311 ◽  
Author(s):  
David J. Press ◽  
Thomas G. Back

A series of o-(hydroxymethyl)phenyl selenides containing single or multiple methoxy substituents was synthesized, and the rate at which each compound catalyzed the oxidation of benzyl thiol to its disulfide with excess hydrogen peroxide was measured. This assay provided the means for comparing the relative abilities of the selenides to mimic the antioxidant selenoenzyme glutathione peroxidase. The mechanism for catalytic activity involves oxidation of the selenides to their corresponding selenoxides with hydrogen peroxide, cyclization to spirodioxyselenuranes, followed by reduction with two equivalents of thiol to regenerate the original selenide with concomitant disulfide formation. A single p-methoxy group on each aryl moiety afforded the highest catalytic activity, while methoxy groups in the meta position had little effect compared to the unsubstituted selenide, and o-methoxy groups suppressed activity. The installation of multiple methoxy groups on each aryl moiety provided no improvement. These results can be rationalized on the basis of dominating mesomeric and steric effects of the p- and o-substituents, respectively.


1987 ◽  
Vol 114 (4) ◽  
pp. 497-502 ◽  
Author(s):  
P. Goyens ◽  
J. Golstein ◽  
B. Nsombola ◽  
H. Vis ◽  
J. E. Dumont

Abstract. Myxoedematous endemic cretinism is prevalent in African goitre endemies. It has been related to a thyroid 'exhaustion' atrophy occurring near birth. It is proposed that this might result from the low resistance of a fragile tissue to enhanced H2O2 generation under intense thyroid stimulation by thyrotropin. In support of this hypothesis, low selenium and glutathione peroxidase serum levels have been found in the African endemic area of the Idjwi Island (Kivu, Zaire). Serum selenium and plasma glutathione peroxidase were lower in the area of high endemicity of goitre and cretinism (Northern part of the Island). However, only the former difference is statistically significant. These data thus suggest a role of oligoelements and oxygen toxicity in the pathogenesis of endemic cretinism.


1996 ◽  
Vol 320 (3) ◽  
pp. 891-895 ◽  
Author(s):  
Giovanna BERMANO ◽  
John R. ARTHUR ◽  
John E. HESKETH

Selenium is an essential nutrient and synthesis of selenoproteins is affected by limited selenium supply. During selenium deficiency there is a differential regulation of selenoprotein synthesis and gene expression; for example, there is a decrease in abundance of mRNA for cytosolic glutathione peroxidase (cGSH-Px) and a preservation of mRNA for phospholipid-hydroperoxide glutathione peroxidase (PHGSH-Px). This difference is not due to an alteration in the rate of transcription but might reflect differences in translation. The aim of the present work was to assess the role of cGSH-Px and PHGSH-Px 3´ untranslated regions (UTRs) in the regulation of selenoprotein mRNA stability and translation by using H4-II-E-C3 cells transfected with different constructs containing a type I iodothyronine deiodinase-coding region linked to different selenoprotein mRNA 3´ UTRs. Translational efficiency results showed that the efficiency of the 3´ UTRs in permitting selenocysteine incorporation is similar in selenium-replete conditions but, when selenium is limiting, the 3´ UTR of cGSH-Px is less efficient than the 3´ UTR of PHGSH-Px. The results suggest that the 3´ UTR of these selenoprotein mRNA species influences their extent of translation when selenium levels are low. The different sensitivity of the 3´ UTRs to selenium deficiency can explain the differential effect that selenium deficiency has on cGSH-Px and PHGSH-Px activity and mRNA levels, stability and translation. This might be partly responsible for channelling selenium for synthesis of PHGSH-Px rather than cGSH-Px.


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