scholarly journals Effect of vitamin E- and selenium-deficiency on rat liver chemiluminescence

1987 ◽  
Vol 242 (2) ◽  
pp. 383-386 ◽  
Author(s):  
C G Fraga ◽  
R F Arias ◽  
S F Llesuy ◽  
O R Koch ◽  
A Boveris
Keyword(s):  
Vitamin E ◽  
Glutathione Peroxidase ◽  
Selenium Deficiency ◽  
Serum Levels ◽  
Hepatic Necrosis ◽  
Deficient Diet ◽  
Control Value ◽  
Weanling Rats

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.

Selenium deficiency as a possible factor in the pathogenesis of myxoedematous endemic cretinism

1987 ◽  
Vol 114 (4) ◽  
pp. 497-502 ◽  
Author(s):  
P. Goyens ◽  
J. Golstein ◽  
B. Nsombola ◽  
H. Vis ◽  
J. E. Dumont
Keyword(s):  
Glutathione Peroxidase ◽  
Oxygen Toxicity ◽  
Selenium Deficiency ◽  
Serum Levels ◽  
Serum Selenium ◽  
Endemic Cretinism ◽  
Plasma Glutathione Peroxidase ◽  
Plasma Glutathione ◽  
Low Selenium

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.

Metabolic and functional defects in selenium deficiency

1981 ◽  
Vol 294 (1071) ◽  
pp. 105-117 ◽  
Keyword(s):  
Hydrogen Peroxide ◽  
Vitamin E ◽  
Glutathione Peroxidase ◽  
Membrane Lipids ◽  
Selenium Deficiency ◽  
Human Nutrition ◽  
Keshan Disease ◽  
Lipid Hydroperoxides ◽  
Membrane Phospholipids

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.

Nutritional Hepatic Necrosis in Beef Cattle “Sawdust Liver”

1966 ◽  
Vol 3 (4) ◽  
pp. 379-400 ◽  
Author(s):  
Glen C. Todd ◽  
Lennart Krook
Keyword(s):  
Fatty Acids ◽  
Vitamin E ◽  
Selenium Deficiency ◽  
Diagnostic Value ◽  
Hepatic Necrosis ◽  
Common Denominator ◽  
Liver Necrosis ◽  
Liver And Kidney ◽  
Tissue Changes ◽  
The Common

A histologic examination of spontaneous cases of sawdust livers in cattle indicated that the focal liver necrosis was an expression of vitamin E-selenium deficiency. The condition was reproduced in Hereford steers by feeding a diet rich in polyunsaturated fatty acids and poor in protein, vitamin E. and selenium. Lesions also occurred in the kidney, heart, skeletal muscled and pylorus. Addition of dictary protein or injection of selenium partially prevented the condition. Cellular anoxia with formation of hyalinc bodies in the liver and kidney was considered to be the common denominator of the degenerative changes. Due to the relatively mild tissue changes, plasma GOT and OCT determinations were found to be of no diagnostic value.

scholarly journals The role of selenium and vitamin E in a Transylvanian enzootic equine recurrent rhabdomyolysis syndrome

2021 ◽  
Author(s):  
Csaba Attila Kósa ◽  
Krisztina Nagy ◽  
Ottó Szenci ◽  
Boglárka Baska-Vincze ◽  
Emese Andrásofszky ◽  
...  
Keyword(s):  
Vitamin E ◽  
Serum Vitamin ◽  
Selenium Deficiency ◽  
Selenium Concentration ◽  
Severe Form ◽  
Serum Selenium ◽  
Muscle Enzymes ◽  
Affected Area ◽  
Recurrent Rhabdomyolysis

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.

TRANSAMINATION IN MUSCULAR DYSTROPHY AND THE EFFECT OF EXOGENOUS GLUTAMATE: A STUDY ON VITAMIN E DEFICIENT RABBITS, AND MICE WITH HEREDITARY DYSTROPHY

1963 ◽  
Vol 41 (1) ◽  
pp. 1423-1432 ◽  
Author(s):  
Roland O. Laferté ◽  
Harris Rosenkrantz ◽  
Louis Berlinguet
Keyword(s):  
Body Weight ◽  
Vitamin E ◽  
Muscular Dystrophy ◽  
Glutamic Acid ◽  
Alanine Transaminase ◽  
Deficient Diet ◽  
Terminal Stage ◽  
Weight Losses

A study of transaminase enzymes in various tissues of different species was carried out. Rabbits were fed with a vitamin E deficient diet. Controls receiving vitamin E were maintained on the same diet. Animals were killed at intervals and the glutamic-aspartic transaminase (GOT) and the glutamic-alanine transaminase (GPT) levels were determined in the muscle, blood, and liver.Mice with hereditary muscular dystrophy and normal litter mates which served as controls were killed at different stages of the disease and GPT and GOT levels were also determined in the muscle, blood, and liver.Important variations between the two types of dystrophy were noticed. Variations in the levels of GPT and GOT were also significant in blood and liver of dystrophic rabbits.Exogenous glutamic acid was injected to vitamin E deprived rabbits. Body weight losses and the onset of the terminal stage of the disease were much postponed when compared to the vitamin E deprived rabbits which did not receive glutamic acid.A discussion of the possible role of glutamic acid in muscular dystrophy of vitamin E deprived rabbits is presented.

scholarly journals Effect of dietary methionine on tissue selenium and glutathione peroxidase (EC 1.11.1.9) activity in rats given selenomethionine

1988 ◽  
Vol 60 (1) ◽  
pp. 57-68 ◽  
Author(s):  
Ingo H. Waschulewski ◽  
Roger A. Sunde
Keyword(s):  
Glutathione Peroxidase ◽  
Active Form ◽  
Lower Percentage ◽  
Deficient Diet ◽  
Treatment Groups ◽  
Weanling Rats ◽  
Tissue Selenium

1. The effect of dietary methionine on the utilization of selenium from dietary selenomethionine ([Se]Met) for tissue Se deposition and for glutathione peroxidase (EC 1.11.1.9; GSH-Px) synthesis was studied in male weanling rats.2. When rats were given 0.5 mg Se as [Se]Met/kg diet supplemented with 0, 4 or 9 g methionine/kg, Se in plasma, erythrocytes, liver and muscle increased significantly over the 20 d period for all methionine-treatment groups. The increases in erythrocyte and muscle Se, however, were significantly higher in rats fed on the methionine-deficient diet compared with the methionine-supplemented diets.3. In contrast to the increases in tissue Se, GSH-Px activity in liver, plasma and muscle decreased in methionine-deficient rats given 0.5 mg Se as [Se]Met/kg whereas GSH-Px activity was maintained or increased in rats supplemented with methionine.4. The percentage of tissue Se associated with GSH-Px was calculated from the measured Se concentration and GSH-Px activity. A significantly lower percentage of Se was associated with GSH-Px in methionine-deficient rats compared with methionine-supplemented rats.5. These results show that Se from dietary [Se]Met is preferentially incorporated into body proteins rather than used for GSH-Px synthesis when methionine is limiting in the diet.6. These results further suggest that [Se]Met might not be the optimum Se compound to use for Se supplementation because metabolism of dietary [Se]Met to a biochemically active form, such as GSH-Px, was impaired when [Se]Met was provided in diets low in methionine.

scholarly journals Some effects of selenium deficiency on glutathione peroxidase (EC 1.11.1.9) activity and tissue pathology in rainbow trout (Salmo gairdneri)

1986 ◽  
Vol 55 (2) ◽  
pp. 305-311 ◽  
Author(s):  
J. G. Bell ◽  
B. J. S. Pirie ◽  
J. W. Adron ◽  
C. B. Cowey
Keyword(s):  
Endoplasmic Reticulum ◽  
Rainbow Trout ◽  
Weight Gain ◽  
Vitamin E ◽  
Glutathione Peroxidase ◽  
Glutathione Transferase ◽  
Selenium Deficiency ◽  
Salmo Gairdneri ◽  
Selenium Content ◽  
Glutathione Peroxidase Activity

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.

scholarly journals Clinical study of experimentally induced vitamin E and selenium deficiency in Awassi ewes and their newborn lambs

2012 ◽  
Vol 36 (2) ◽  
pp. 158-162
Author(s):  
H. K. Abood
Keyword(s):  
Body Weight ◽  
Clinical Study ◽  
Vitamin E ◽  
Clinical Signs ◽  
Selenium Deficiency ◽  
Serum Selenium ◽  
Deficient Diet ◽  
Sheep Industry ◽  
Experimental Induction ◽  
Deficient Group

Experimental induction of vitamin E and selenium deficiency by deficient diet was carried out on Awassi ewes and their newborn lambs. The clinical signs were characterized by sudden death in 4 lambs out of 14 lambs in deficient group and other lambs showed a variable signs included inability to suckle, arched back, weakness, dullness, emaciation and recumbency. Serum selenium and vitamin E levels of these lambs were 0.01 ppm and 0.34 mg/L respectively. The clinical signs in ewes included loss of body weight and loss of wool, Weakness, dullness and recumbency. Serum selenium and vitamin E levels of these ewes were 0.02 ppm and 0.61mg/L respectively. It was concluded that vitamin E and selenium are essential antioxidants and their deficiency exposes the sheep industry to many serious losses.

6.3 The Development and Effects of Selenium Deficiency

1983 ◽  
Vol 7 ◽  
pp. 128-128
Author(s):  
J. R. Arthur ◽  
R. Boyne
Keyword(s):  
Skeletal Muscle ◽  
Vitamin E ◽  
Glutathione Peroxidase ◽  
Heart Muscle ◽  
Clinical Symptoms ◽  
Selenium Deficiency ◽  
Focal Lesions ◽  
Vitamin E Deficiency ◽  
Vitamin E Status ◽  
Cattle And Sheep

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.

scholarly journals On the relationship between vitamin A and vitamin E in the rat

1968 ◽  
Vol 22 (1) ◽  
pp. 133-143 ◽  
Author(s):  
M. A. Cawthorne ◽  
J. Bunyan ◽  
A. T. Diplock ◽  
Elspeth A. Murrell ◽  
J. Green
Keyword(s):  
Weight Gain ◽  
Vitamin E ◽  
Vitamin A ◽  
Methyl Esters ◽  
Tocopheryl Acetate ◽  
Cod Liver Oil ◽  
Deficient Diet ◽  
Weanling Rats ◽  
The Relationship

1. The effect of vitamin E on the metabolism, utilization and storage of vitamin A has been studied in the rat.2. Male weanling rats were given a vitamin A-deficient, vitamin E-deficient diet until growth had ceased for 3 days, and each rat was then given 50 i.u. vitamin A palmitate. The rats were divided into four groups and given the diet with the addition of 10% methyl oleate or 10% cod-liver oil methyl esters, or either of these diets supplemented with 100 ppm D-α-tocopheryl acetate. There was no increase in maximum weight-gain response in the two groups given vitamin E. There was a significantly lower weight-gain response in the groups given cod-liver oil methyl esters. This effect was not influenced by the presence of vitamin E in the diet.3. Weanling rats of both sexes were made deficient in vitamins A and E and then divided into two groups. One group received, every other day, 1·75 i.u. vitamin A palmitate and 0·6 mg D-α-tocopherol given together; the second group received the two vitamins, in the same amounts, on alternate days. After 28 days there was no difference in the growth of the two groups of rats, irrespective of sex.4. Vitamin A-depleted, vitamin E-deficient rats were given 17·51 μg ‘14C-carbinol’retinyl acetate and then a vitamin A-deficient, vitamin E-deficient diet or that diet supplemented with 100 ppm D-α-tocopheryl acetate. After 6 days, the total remaining ‘14C’retinol and its lipidsoluble metabolites were measured in the carcasses of the rats. Vitamin E administration did not affect the metabolism of the vitamin A dose or its effect on growth.5. Vitamin E-deficient rats were given vitamin A until their liver reserves exceeded 30000 i.u. and were then divided into two groups. One group received a diet deficient in vitamins A and E and the other received, in addition to this diet, a weekly oral supplement of 1 mg D-α-tocopheryl acetate. The vitamin E supplement significantly decreased the rate of vitamin A depletion from the liver during the next 6 weeks. This effect, which was not found to occur when the initial liver reserves were only 3000 i.u., suggests a role for vitamin E in connexion with the capacity of the liver to bind vitamin A.6. The relationship between vitamin A and vitamin E in vivo cannot, in the light of these results, be regarded as that between an antioxidant and a peroxidizable substrate.

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