Biochemical Alterations in the Skeletal Muscle of Vitamin E Deficient Rats

1971 ◽  
Vol 49 (11) ◽  
pp. 1202-1208 ◽  
Author(s):  
Naranjan S. Dhalla ◽  
Margaret Fedelesova ◽  
Ivan Toffler
Keyword(s):  
Skeletal Muscle ◽  
Vitamin E ◽  
Energy State ◽  
Muscle Metabolism ◽  
Creatine Phosphate ◽  
Normal Diet ◽  
Deficient Diet ◽  
Biochemical Alterations ◽  
Leg Muscles ◽  
Glycerophosphate Dehydrogenase

Rats were fed a vitamin E deficient diet for 5–10 weeks and the energy state of the hind leg muscle was examined. Both creatine phosphate and ATP were decreased by 64 and 22% of the control values, respectively, in the skeletal muscles of rats on the vitamin E deficient diet for 10 weeks, whereas ADP was increased by more than 100% without any significant changes in the level of AMP. The ratios ATP/ADP and ATP/AMP also declined markedly in the hind leg muscles of the rats on the vitamin E deficient diet for 10 weeks. The concentrations of NAD+ and NADPH decreased, whereas no significant changes in the levels of NADH and NADP+ were observed in the muscles of vitamin E deficient animals. Feeding a normal diet for 4 weeks to rats previously on the vitamin E deficient diet was found to restore the energy state of the muscle towards normal. Although no changes in the ultrastructure of the skeletal muscle were apparent, the levels of lactate and pyruvate as well as the lactate/pyruvate ratio were increased in vitamin E deficiency. The activities of lactate dehydrogenase and malate dehydrogenase were decreased whereas α-glycerophosphate dehydrogenase activity did not change significantly. These results indicate a dramatic alteration in skeletal muscle metabolism of vitamin E deficient rats. It is suggested that such a change may partly be due to a defect in the process of energy production.

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.

Role of free radicals in catecholamine-induced cardiomyopathy

1982 ◽  
Vol 60 (11) ◽  
pp. 1390-1397 ◽  
Author(s):  
P. K. Singal ◽  
N. Kapur ◽  
K. S. Dhillon ◽  
R. E. Beamish ◽  
N. S. Dhalla
Keyword(s):  
Free Radicals ◽  
Vitamin E ◽  
Creatine Phosphate ◽  
Normal Diet ◽  
Ultrastructural Changes ◽  
Antioxidant Vitamin ◽  
Deficient Diet ◽  
Increased Sensitivity ◽  
Increase Membrane Permeability ◽  
Induced Changes

Effects of an antioxidant, vitamin E, and a membrane stabilizing agent, zinc, were examined on the isoproterenol-induced changes in the rat myocardium. Isoproterenol treatment (80 mg/kg given over 2 days in two equal doses) caused arrhythmias and 25% mortality within 24 h of the last injection. The ultrastructural changes in the subendocardium and in focal areas of the subepicardium included swelling of mitochondria, loss of myofibrils, cell necrosis, fibrosis, and infiltration of the affected areas by polymorphonucleocytes. Both creatine phosphate and adenosine triphosphate levels were markedly decreased in hearts from isoproterenol-treated animals. Pretreatment of the animals with vitamin E (10 mg∙kg−1∙day−1 for 2 weeks) or zinc (10 mg/kg ZnSO4, twice a day for 7 days) prevented these deleterious effects of isoproterenol. Animals maintained on vitamin E deficient diet for 8 weeks were found to be more sensitive to isoproterenol-induced changes and this increased sensitivity was reversed by a 2-week feeding of the animals on the normal diet coupled with vitamin E treatment. Based on the data obtained in this study it is proposed that catecholamine-induced changes may involve free radicals, which by promoting lipid peroxidation may increase membrane permeability and lead to the development of cardiomyopathy.

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.

Interaction of factors determining oxygen uptake at the onset of exercise

1999 ◽  
Vol 86 (4) ◽  
pp. 1101-1113 ◽  
Author(s):  
M. E. Tschakovsky ◽  
R. L. Hughson
Keyword(s):  
Skeletal Muscle ◽  
Redox Potential ◽  
Energy State ◽  
Muscle Metabolism ◽  
Enzyme Activation ◽  
Transport Mechanisms ◽  
Atp Production ◽  
Theoretical Approaches ◽  
Considerable Debate ◽  
Adaptation To Exercise

Considerable debate surrounds the issue of whether the rate of adaptation of skeletal muscle O2 consumption (Q˙o 2) at the onset of exercise is limited by 1) the inertia of intrinsic cellular metabolic signals and enzyme activation or 2) the availability of O2 to the mitochondria, as determined by an extrinsic inertia of convective and diffusive O2 transport mechanisms. This review critically examines evidence for both hypotheses and clarifies important limitations in the experimental and theoretical approaches to this issue. A review of biochemical evidence suggests that a given respiratory rate is a function of the net drive of phosphorylation potential and redox potential and cellular mitochondrial[Formula: see text](Pmito o 2). Changes in both phosphorylation and redox potential are determined by intrinsic metabolic inertia. Pmito o 2is determined by the extrinsic inertia of both convective and diffusive O2 transport mechanisms during the adaptation to exercise and the rate of mitochondrial O2 utilization. In a number of exercise conditions, Pmito o 2appears to be within a range capable of modulating muscle metabolism. Within this context, adjustments in the phosphate energy state of the cell would serve as a cytosolic “transducer,” linking ATP consumption with mitochondrial ATP production and, therefore, O2 consumption. The availability of reducing equivalents and O2would modulate the rate of adaptation ofQ˙o 2.

Effect of Vitamin E Deficient Diet Upon Skeletal Muscle

1938 ◽  
Vol 38 (5) ◽  
pp. 665-667 ◽  
Author(s):  
G. C. Knowlton ◽  
H. M. Hines
Keyword(s):  
Skeletal Muscle ◽  
Vitamin E ◽  
Deficient Diet

scholarly journals Untargeted Metabolomic Characteristics of Skeletal Muscle Dysfunction in Rabbits Induced by a High Fat Diet

Animals ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 1722
Author(s):  
Huimei Fan ◽  
Yanhong Li ◽  
Jie Wang ◽  
Jiahao Shao ◽  
Tao Tang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
High Fat Diet ◽  
Metabolic Diseases ◽  
Muscle Metabolism ◽  
Principal Component ◽  
Oxidative Capacity ◽  
Ultra Performance Liquid Chromatography ◽  
Normal Diet ◽  
High Fat ◽  
Tissue Samples

Type 2 diabetes and metabolic syndrome caused by a high fat diet (HFD) have become public health problems worldwide. These diseases are characterized by the oxidation of skeletal muscle mitochondria and disruption of insulin resistance, but the mechanisms are not well understood. Therefore, this study aims to reveal how high-fat diet causes skeletal muscle metabolic disorders. In total, 16 weaned rabbits were randomly divided into two groups, one group was fed a standard normal diet (SND) and the other group was fed a high fat diet (HFD) for 5 weeks. At the end of the five-week experiment, skeletal muscle tissue samples were taken from each rabbit. Untargeted metabolomic analysis was performed using ultra-performance liquid chromatography combined with mass spectrometry (UHPLC-MS/MS). The results showed that high fat diet significantly altered the expression levels of phospholipids, LCACs, histidine, carnosine, and tetrahydrocorticosterone in skeletal muscle. Principal component analysis (PCA) and least squares discriminant analysis (PLS-DA) showed that, compared with the SND group, skeletal muscle metabolism in HFD group was significantly up-regulated. Among 43 skeletal muscle metabolites in the HFD group, phospholipids, LCACs, histidine, carnosine, and tetrahydrocorticosteroids were identified as biomarkers of skeletal muscle metabolic diseases, and may become potential physiological targets of related diseases in the future. Untargeted metabonomics analysis showed that high-fat diet altered the metabolism of phospholipids, carnitine, amino acids and steroids in skeletal muscle of rabbits. Notably, phospholipids, LCACs, histidine, carnopeptide, and tetrahydrocorticosteroids block the oxidative capacity of mitochondria and disrupt the oxidative capacity of glucose and the fatty acid-glucose cycle in rabbit skeletal muscle.

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

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.

scholarly journals Regulation of metabolism: the work-to-rest transition in skeletal muscle

2016 ◽  
Vol 310 (8) ◽  
pp. E633-E642 ◽  
Author(s):  
David F. Wilson
Keyword(s):  
Skeletal Muscle ◽  
Oxidative Phosphorylation ◽  
Energy State ◽  
Creatine Phosphate ◽  
Steady States ◽  
Rate Of Change ◽  
Similar Time ◽  
Oxygen Gradients ◽  
Regulation Of Metabolism ◽  
Time Courses

The behavior of oxidative phosphorylation predicted by a model for the mechanism and kinetics of cytochrome c oxidase is compared with the experimentally observed behavior during the work-to-rest transition in skeletal muscle. For both experiment and model, when work stops, the increase in creatine phosphate and decrease in creatine and inorganic phosphate concentrations ([CrP], [Cr], and [Pi]) begin immediately. The rate of change for each is maximal and then progressively slows as the increasing energy state ([ATP]/[ADP][Pi]) suppresses the rate of oxidative phosphorylation. The time courses can be reasonably fitted to single exponential curves with similar time constants. The energy state in the working and resting steady states at constant Po2 are dependent on the intramitochondrial [NAD+]/[NADH], mitochondrial content, and size of the creatine pool ([CrP] + [Cr]). The rate of change in [CrP] is linearly correlated with [CrP] and with [Pi] and [Cr]. The time constant for [CrP] increase in the resting and working steady states, and the rate of decrease in oxygen consumption are similarly dependent on the Po2 in the inspired gas (experimental) or tissue Po2 (model). Myoglobin strongly buffers intracellular Po2 below ∼15 torr, truncating the low end of the oxygen distribution in the tissue and suppressing intra- and intermyocyte oxygen gradients. The predictions of the model are consistent with the experimental data throughout the work/rest transition, providing valuable insights into the regulation of cellular and tissue metabolism.

Liver Histological Improvement After Administration of High-Dose Vitamin C in Guinea Pig with Nonalcoholic Steatohepatitis

2018 ◽  
Vol 88 (5-6) ◽  
pp. 263-269
Author(s):  
Seong-Hoon Park ◽  
A Lum Han ◽  
Na-Hyung Kim ◽  
Sae-Ron Shin
Keyword(s):  
Liver Biopsy ◽  
Vitamin C ◽  
Nonalcoholic Steatohepatitis ◽  
Guinea Pigs ◽  
Normal Diet ◽  
High Dose ◽  
Biochemical Tests ◽  
Deficient Diet ◽  
Histological Improvement ◽  
Vit C

Abstract. Background: Vitamin C is a strong antioxidant, and the health effects of vitamin C megadoses have not been validated despite the apparent health benefits. Therefore, the present study sought to confirm the effects of vitamin C megadoses. Materials and Methods : Four groups of six guinea pigs were used. Each group was fed one of the following diets for three weeks: normal diet, methionine choline-deficient diet, methionine choline-deficient diet + vitamin C megadose (MCD + vit C 2.5 g/kg/day), and methionine-choline deficient diet + ursodeoxycholic acid (MCD + UDCA 30 mg/kg/day). The MCD diet was given to induce nonalcoholic steatohepatitis, and UDCA was used to treat nonalcoholic steatohepatitis. Three weeks after initial diet administration, the results of biochemical tests and liver biopsy were compared between the groups. Results: The cytoplasm state was similar in the MCD + vit C and MCD + UDCA groups, exhibiting clearing of the cytoplasm and ballooning degeneration. However, macrovesicular steatosis was not observed in the MCD + vit C group. Aspartate transaminase and alanine transaminase were elevated significantly following vitamin C administration. Conclusions: The present study confirmed that alone vitamin C megadoses are potential remedies for nonalcoholic steatohepatitis, based on the liver biopsy results of guinea pigs that were unable to synthesize vitamin C.

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