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.

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 Role of Vitamin E on Indomethacin induced low pH of Seminal Fluid in Long Evans Rats

1970 ◽  
Vol 8 (1) ◽  
pp. 13-15
Author(s):  
Md Jahangir Alam ◽  
Humaira Naushaba ◽  
Uttam Kumar Paul ◽  
Tahmina Begum ◽  
Sunjida Shahriah ◽  
...  
Keyword(s):  
Body Weight ◽  
Vitamin E ◽  
Seminal Fluid ◽  
Low Ph ◽  
The Other ◽  
Testicular Damage ◽  
Other Hand ◽  
Long Evans ◽  
Different Doses

Context: Indomethacin is the most commonly and widely used nonsteroidal antinflammatory analgesic and antipyretic drug. Though it is effective drug in various diseases, indomethacin causes inhibition of spermatogenesis by lowering the pH of seminal fluid leading to infertility. On the other hand, vitamin E enhances spermatogenesis by increasing pH of the seminal fluid. Therefore, the present study was designed to observe the protective role of vitamin E on indomethacin induced low pH of seminal fluid in testicular damage. Objective: To observe the effects of vitamin E on indomethacin induced low pH of seminal fluid in testicular damage in Long Evans rats. Study design: An experimental study. Place and period of study: The study was carried out in the Department of Anatomy, Sir Salimullah Medical College, Dhaka in the period of August, 2005 to June, 2006. Materials and methods: Eightyfour mature Long Evans male rats were divided into four groups (I, II, III and IV). The rats of group I, II and III were treated with indomethacin at different doses and duration. Group IV rats were treated with indomethacin plus vitamin E at different doses for 49 days. The pH of seminal fluid were measured biochemically. Results: There was significant reduction (P<0.001) of pH of seminal fluid when the rats were treated with indomethacin at low (2 mg/kg body weight/day) and high (10 mg/kg body weight/day) doses for 7, 14 and 42 days, respectively. On the other hand, rats treated with indomethacin plus vitamin E for 49 days showed increase in pH of seminal fluid compared to other groups (P<0.001). Conclusion: It can be concluded from the study that vitamin E has potential role in the prevention of the antispermatogenic effects of indomethacin by increasing the pH of seminal fluid. Key words: seminal fluid; indomethacin; vitamin E   DOI: 10.3329/bja.v8i1.6103 Bangladesh Journal of Anatomy January 2010, Vol. 8 No. 1 pp. 13-15

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.

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.

Physiological and Histological Study to the Effects of Monosodium Glutamate in Laboratory male Rats and the protective role of vitamin E

2019 ◽  
Vol 10 (02) ◽  
Author(s):  
Genan Musheer Ghaib AL-Khatawi ◽  
Mohammed R S AL-Attabi ◽  
Ali Fayadh Bargooth
Keyword(s):  
Body Weight ◽  
Vitamin E ◽  
Low Density Lipoprotein ◽  
Monosodium Glutamate ◽  
Density Lipoprotein ◽  
Male Rats ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Liver And Kidney

The current study was conducted at the Department of Biology, College of Science, Wasit University to investigate physiological and histological effect monosodium glutamate in laboratory male rats, preventive role of vitamin E. This study was carried out in Laboratories of College of Science, Wasit University, AL- Shaheed Dr. Fairooz Hospitals, from November 2017 to April 2018.The study included twenty-four and divided into four groups (six rats per group). the first group severe as a control group orally dosed with distilled water, and treated the second group (100 mg/kg b.w. Monosodium glutamate for 30 days, and the third group were dosed orally 200 mg/kg of b.w. for 30 days, either The fourth group were dosed with a mixture of Monosodium glutamate 200mg/kg and vitamin E 100 mg/kg of body weight for 30 days. after the trial period has been sacrificing animals for testing and chemical standards physiological and histological. As are result of by exposure to Monosodium glutamate in blood serum are negatively biochemical whole height of the level of serum cholesterol, triglycerides, Low-density lipoprotein, very- low density lipoprotein, liver enzymes, AST, ALT, ALP, creatinine level, urea serum, further more we noticed a decrease in high density lipoprotein. The preventive treatment resulted in vitamin E 100mg/kg b.w. with Monosodium glutamate 200 mg/kg b.w. (p≤ 0.05) in body weight and relative weights of organs (liver and kidney). We noticed a higher moral when treatment with vitamin E with Monosodium glutamate 100 mg/kg in high- density lipoprotein, while serum cholesterol level decrease, triglycerides, Low-density lipoprotein, very- low density lipoprotein. And liver and kidney functions have improved by low Enzyme AST, ALT, ALP, creatinine and urea serum level. Histological examination revealed that the liver and kidneys, of rats exposed 100, 200 mg/kg of Monosodium glutamate has been adversely affected by exposure to Monosodium glutamate. Whereas, the histological of the liver of animals treated with vitamin E with Monosodium glutamate natural pictures showed improvement. These results demonstrate that MSG toxic effects on the liver and kidney tissue. The more toxic than salt rate too. The study recommends to avoid using MSG as food additives and food for animals because of the toxic effects of this salt.

ROLE OF VITAMIN E IN THE PREVENTION OF MUSCULAR DYSTROPHY IN GUINEA PIGS REARED ON SYNTHETIC RATIONS

Science ◽  
1939 ◽  
Vol 90 (2326) ◽  
pp. 89-89 ◽  
Author(s):  
N. Shimotori ◽  
G. A. Emerson ◽  
H. M. Evans
Keyword(s):  
Vitamin E ◽  
Muscular Dystrophy ◽  
Guinea Pigs

Effect of Phytol on the Incidence of Muscular Dystrophy in Rabbits

1972 ◽  
Vol 50 (2) ◽  
pp. 171-172 ◽  
Author(s):  
M. Hidiroglou ◽  
K. J. Jenkins
Keyword(s):  
Vitamin E ◽  
Muscular Dystrophy ◽  
Deficient Diet ◽  
Vitamin E Supplementation

In an experiment with 60 rabbits fed a vitamin E deficient diet, 1% of phytol was ineffective in prevention of muscular dystrophy, whereas vitamin E supplementation at 100 p.p.m. completely prevented onset of the disease. This observation with rabbits contrasts with the reported antidystrophic activity of phytol in chicks.

scholarly journals Cellular senescence-mediated exacerbation of Duchenne muscular dystrophy

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Hidetoshi Sugihara ◽  
Naomi Teramoto ◽  
Katsuyuki Nakamura ◽  
Takanori Shiga ◽  
Taku Shirakawa ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Body Weight ◽  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Muscle Strength ◽  
Progenitor Cells ◽  
Satellite Cells ◽  
Muscle Regeneration ◽  
Mesenchymal Progenitor Cells

Abstract Duchenne muscular dystrophy (DMD) is a progressive disease characterised by chronic muscle degeneration and inflammation. Our previously established DMD model rats (DMD rats) have a more severe disease phenotype than the broadly used mouse model. We aimed to investigate the role of senescence in DMD using DMD rats and patients. Senescence was induced in satellite cells and mesenchymal progenitor cells, owing to the increased expression of CDKN2A, p16- and p19-encoding gene. Genetic ablation of p16 in DMD rats dramatically restored body weight and muscle strength. Histological analysis showed a reduction of fibrotic and adipose tissues invading skeletal muscle, with increased muscle regeneration. Senolytic drug ABT263 prevented loss of body weight and muscle strength, and increased muscle regeneration in rats even at 8 months—the late stage of DMD. Moreover, senescence markers were highly expressed in the skeletal muscle of DMD patients. In situ hybridization of CDKN2A confirmed the expression of it in satellite cells and mesenchymal progenitor cells in patients with DMD. Collectively, these data provide new insights into the integral role of senescence in DMD progression.

Influence of a Protein-Free Diet on the Immediate and Latent Effects of Stilbestrol

1957 ◽  
Vol 189 (3) ◽  
pp. 441-446 ◽  
Author(s):  
Stanley R. Glasser
Keyword(s):  
Body Weight ◽  
Nitrogen Loss ◽  
Body Weight Loss ◽  
Liver Fat ◽  
Treated Animal ◽  
Liver Protein ◽  
Deficient Diet ◽  
Adequate Diet ◽  
Weight Losses ◽  
Protein Deficient Diet

The absence of protein from the diet of stilbestrol-treated rats modified, largely quantitatively the response to the hormone. Stilbestrol, per se, induced a body weight loss which was greater in the protein-depleted than in the protein-fed animal. Recovery on an adequate protein diet, after withdrawal of the hormone permitted an immediate recouping of body weight losses, whereas animals on the protein-deficient diet did not recover body weight losses. Stilbestrol administration increased excretion of nitrogen indirectly by restriction of food intake. This nitrogen loss was augmented by protein depletion. The marked retention of nitrogen by animals recovering on an adequate diet was more pronounced in the treated animal but rats continued on the protein-deficient diet maintained a negative nitrogen balance. The absence of protein from the diet diminished the anticatabolic influence of stilbestrol on total liver protein. Recovery on the basal diet allowed the repletion of liver protein but further decreases in liver protein concentration followed recovery on the deficient diet. A marked increase in the concentration of liver fat appeared concomitantly with the progressive depletion of liver protein in both treated and untreated groups.

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