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.

scholarly journals The Effect of Experimentally Induced Vitamin E and Selenium Deficiency on Erythrocytes Osmotic Fragility and Phagocytosis in Pregnant Awassi Ewes and Their Newborn Lamb

2013 ◽  
Vol 37 (2) ◽  
pp. 188-191
Author(s):  
A. M. H. Judi
Keyword(s):  
Vitamin E ◽  
Saline Solution ◽  
Osmotic Fragility ◽  
Selenium Deficiency ◽  
Phagocytic Index ◽  
Control Group ◽  
Deficient Diet ◽  
Newborn Lamb ◽  
Experimental Induction ◽  
Study Results

Experimental induction of vitamin E and selenium deficiency using deficient diet was carried out on fourteen pregnant Awassi ewes and their newborn lambs to study the effect of the deficiency on erythrocytes osmotic fragility and phagocytosis. From the fourteen deficient ewes, seven were vaccinated with Rev I vaccine and seven ewes as control group, and their newborn lambs were used in the study. Results were showed increased in the concentration of saline solution in start and complete erythrocyte hemolysis in deficient lambs (0.52 ± 0.01 and 0.54 ± 0.01) and (0.42 ± 0.01 and 0.44 ± 0.00) respectively and in deficient ewes (0.53 ± 0.01 and 0.54 ± 0.01) and (0.43 ± 0.01 and 0.44 ± 0.00) respectively. Results showed a low phagocytic index in deficient lambs (9.40 ± 0.87 and 10.60 ± 1.16) and in deficient ewes (12.14 ± 0.85 and 12.42 ± 0.75) compared to phagocytic index in control lambs (43.85±0.91) and in control ewes (43.14 ±0.91).

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 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.

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 (6) ◽  
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.

Biochemical Basis of Heart Function. IV. Energy Metabolism and Calcium Transport in Hearts of Vitamin E Deficient Rats

1971 ◽  
Vol 49 (10) ◽  
pp. 909-918 ◽  
Author(s):  
Margaret Fedelesova ◽  
Prakash V. Sulakhe ◽  
John C. Yates ◽  
Naranjan S. Dhalla
Keyword(s):  
Vitamin E ◽  
Sarcoplasmic Reticulum ◽  
Heart Function ◽  
Adenine Nucleotides ◽  
Creatine Phosphate ◽  
Normal Diet ◽  
Vitamin E Deficiency ◽  
Deficient Diet ◽  
Cardiac Sarcoplasmic Reticulum ◽  
Biochemical Basis

Feeding a vitamin E deficient diet to rats for 10 weeks was found to decrease myocardial creatine phosphate, ATP, ATP/ADP ratio, NAD+, NADP+, and NADPH, whereas the level of ADP was increased without any changes in the levels of AMP, total adenine nucleotides, NADH, and ATP/AMP ratio. The levels of ATP and pyridine nucleotides were restored fully, whereas creatine phosphate was restored partially on feeding a normal diet for 4 weeks to animals previously on the vitamin E deficient diet for 10 weeks. Vitamin E deficiency was found to increase cardiac lactate, pyruvate, and lactate/pyruvate ratio and decrease the activities of lactate dehydrogenase and malate dehydrogenase. The activity of Na+–K+-stimulated, ouabain-sensitive ATPase was markedly elevated in the hearts of animals on the vitamin E deficient diet. The ATP-dependent calcium accumulation by the sarcoplasmic reticular fraction in the absence and presence of P1 or oxalate was greater in the vitamin E deficient heart. Vitamin E deficiency also increased the Ca2+-stimulated ATPase activity of the cardiac sarcoplasmic reticulum. Although myocardial contractility of the hearts from vitamin E deficient rats was depressed, no damage to the ultrastructures of mitochondria and sarcoplasmic reticulum was apparent. These results indicate marked alterations in myocardial metabolism due to vitamin E deficiency and it is suggested that such changes are due to abnormalities in the processes of both energy production and utilization.

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