Effects of a short period of vitamin E-deficient diet in the turnover of different neurotransmitters in substantia nigra and striatum of the rat

Neuroscience ◽  
1993 ◽  
Vol 53 (1) ◽  
pp. 179-185 ◽  
Author(s):  
A. Castan˜o ◽  
A.J. Herrera ◽  
J. Cano ◽  
A. Machado
Keyword(s):  
Vitamin E ◽  
Substantia Nigra ◽  
Deficient Diet ◽  
Short Period

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.

Effect of short-term vitamin E deficiency on guinea pig skeletal muscle myoglobin

1959 ◽  
Vol 197 (2) ◽  
pp. 491-493 ◽  
Author(s):  
A. D. Bender ◽  
D. D. Schottelius ◽  
B. A. Schottelius
Keyword(s):  
Skeletal Muscle ◽  
Vitamin E ◽  
Guinea Pig ◽  
Guinea Pigs ◽  
Short Term ◽  
Vitamin E Deficiency ◽  
Deficient Diet ◽  
Wet Weight ◽  
Masseter Muscles ◽  
Nitrogen Percentage

Myoglobin concentration was determined in gastrocnemius and masseter muscles of guinea pigs maintained up to 15 days on vitamin E-deficient and vitamin E-supplemented diets. A statistically significant increase in myoglobin was noted in muscles of animals on the deficient diet for 15 days. That the increase was real and not apparent was attested by studies of total nitrogen, noncollagen nitrogen, percentage of solids and muscle wet weight, all of which were the same in control and experimental muscles. Histological sections and creatine excretion studies confirmed the impression of mild, incipient nutritional dystrophy.

scholarly journals Abnormalities of iron metabolism and erythropoiesis in vitamin E- deficient rabbits

Blood ◽  
1978 ◽  
Vol 52 (1) ◽  
pp. 187-195 ◽  
Author(s):  
AC Chou ◽  
GO Jr Broun ◽  
CD Fitch
Keyword(s):  
Skeletal Muscle ◽  
Bone Marrow ◽  
Vitamin E ◽  
Iron Metabolism ◽  
Iron Absorption ◽  
Iron Concentration ◽  
Vitamin E Deficiency ◽  
Deficient Diet ◽  
Plasma Iron ◽  
Erythroid Hyperplasia

Abstract Rabbits fed a vitamin E-deficient diet developed severe muscular dystrophy in 3–4 wk, but they did not become anemic. Nevertheless, reticulocyte counts increased in deficient rabbits (3.2%) compared to control rabbits (0.9%), and erythroid hyperplasia was evident in the bone marrow. Comparing deficient rabbits to controls, the plasma iron concentration was lower (134.4 versus 206.6 microgram/dl); the TIBC was higher (335.9 versus 228.3 microgram/dl); the whole blood protoporphyrin concentration was higher (131.6 versus 81.7 microgram/dl); and the total iron content was lower in spleen (71 versus 153 microgram), higher in skeletal muscle (4956 versus 3054 microgram), and unchanged in bone marrow, liver, and heart. Studies of iron absorption and excretion using 59Fe showed no abnormalities in deficient rabbits. There were abnormalities of ferrokinetics, however. The half-time of disappearance of 59Fe was shorter (100.6 versus 169.4 min), the plasma iron turnover was greater (1.25 versus 0.95 mg/dl blood/day), and the reappearance of 59Fe in circulating erythrocytes at day 9 was greater (77.2% versus 57.2%) in deficient rabbits. Anemia induced by phlebotomy accentuated the abnormal iron metabolism of deficient rabbits, and the animals were unable to correct the anemia. These findings show that vitamin E deficiency in rabbits causes abnormal erythropoiesis associated with abnormal iron metabolism and sequestration of iron in skeletal muscle.

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.

Vitamin E Deficiency Fails to Affect Myocardial Performance During In Vivo Ischemia-Reperfusion

2000 ◽  
Vol 70 (6) ◽  
pp. 293-300 ◽  
Author(s):  
Jeff Coombes ◽  
Scott Powers ◽  
Haydar Demirel ◽  
Karyn Hamilton ◽  
James Jessup ◽  
...  
Keyword(s):  
Vitamin E ◽  
Corn Oil ◽  
Ischemia Reperfusion ◽  
Control Diet ◽  
Cardiac Performance ◽  
In Vivo Model ◽  
Vitamin E Deficiency ◽  
Deficient Diet ◽  
Protein Thiols

Vitamin E content, of cardiac tissue, has been proposed to play a major, role in the damage caused by myocardial ischemia-reperfusion (I-R). Previous studies using in vitro models have examined vitamin E deficiency and I-R-induced myocardial damage with equivocal results. The purpose of this study was to use an in vivo model of myocardial I-R to determine the effects of vitamin E deficiency on myocardial I-R-induced damage. Female Sprague-Dawly rats (4-mo old) were assigned to either: 1) control diet (CON), or 2) vitamin E deficient diet (VE-DEF). The CON diet was prepared to meet AIN-93M standards, which contains 75 IU vitamin E/kg diet. The VE-DEF diet was the AIN-93M diet prepared with tocopherol stripped corn oil and no vitamin E. Following a 14-week feeding period, significant differences (p < 0.05) existed in mean myocardial VE levels between groups (mean values ± SEM: CON = 48.2 ± 3.5; VE-DEF = 12.4 ± 1,4 mug VE/g wet weight). Animals from both experimental groups were subjected to an in vivo I-R protocol consisting of 25 minutes of left coronary artery occlusion followed by 10 minutes of reperfusion. No group differences (p > 0.05) existed in cardiac performance (peak arterial pressure or ventricular work) or the incidence of ventricular arrhythmias during the I-R protocol. VE-DEF animals had significantly higher (p < 0.05) levels of myocardial lipid peroxidation and lower (p < 0.05) protein thiols following I-R compared to the CON animals. These data suggest that although vitamin E deficiency increases oxidative damage resulting from myocardial I-R, it does not affect cardiac performance during the insult.

scholarly journals The Pathogenicity of an EntericCitrobacter rodentiumInfection Is Enhanced by Deficiencies in the Antioxidants Selenium and Vitamin E

2011 ◽  
Vol 79 (4) ◽  
pp. 1471-1478 ◽  
Author(s):  
Allen D. Smith ◽  
Sebastian Botero ◽  
Terez Shea-Donohue ◽  
Joseph F. Urban
Keyword(s):  
Vitamin E ◽  
Control Diet ◽  
Heme Oxygenase 1 ◽  
Mrna Levels ◽  
Deficient Diet ◽  
Adequate Diet ◽  
Cytokines And Chemokines ◽  
Food Borne ◽  
Infiltrating Cells ◽  
Crypt Hyperplasia

ABSTRACTThe pathogenesis of aCitrobacter rodentiuminfection was evaluated in mice fed diets with a single deficiency in either selenium or vitamin E or with a double deficiency in both selenium and vitamin E compared to mice on nutritionally adequate diets. Mice fed the selenium- and vitamin E-deficient diet for 6 weeks had increased loads ofC. rodentiumin the colon and spleen, which were not observed in mice fed either of the singly deficient diets or the adequate diet. Infected mice fed the doubly deficient diet had increased colon crypt hyperplasia and an influx of infiltrating cells along with gross changes to crypt architecture, including ulceration and denuding of the epithelial layer. Cytokine and chemokine mRNA levels in the colon were measured by real-time PCR. Expression of proinflammatory cytokines and chemokines was upregulated on day 12 after infection withC. rodentiumin mice fed the doubly deficient diet compared to mice fed the control diet. Heme oxygenase 1, an enzyme upregulated by oxidative stress, also was more highly induced in infected mice fed the doubly deficient diet. Production ofC. rodentiumantigen-specific IgM and IgG antibodies was not affected by feeding the doubly deficient diet. The results indicated that selenium and vitamin E play an important role in host resistance and in the pathology induced byC. rodentium, an infection that mimics disease caused by common food-borne bacterial pathogens in humans.

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