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.

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.

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.

Impaired energy metabolism in rat myocardium during phosphate depletion

1982 ◽  
Vol 242 (6) ◽  
pp. F699-F704 ◽  
Author(s):  
N. Brautbar ◽  
R. Baczynski ◽  
C. Carpenter ◽  
S. Moser ◽  
P. Geiger ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Adenine Nucleotides ◽  
Creatine Phosphate ◽  
Inorganic Phosphorus ◽  
High Energy ◽  
Deficient Diet ◽  
Myocardial Energetics ◽  
Phosphate Depletion ◽  
Myocardial Biopsies ◽  
Mitochondrial Capacity

The effects of phosphate depletion (PD) of 4, 8, and 12 wk duration on myocardial energy metabolism were studied in rats fed a phosphate-deficient diet and compared with rats pair-fed a normal phosphate diet. Myocardial biopsies were examined for high-energy phosphate bonds. The results show that PD causes a significant reduction in myocardial concentration of inorganic phosphorus at 4 wk of PD and creatine phosphate at 8 wk of PD, while adenine nucleotides were significantly reduced only after 12 wk of PD. The changes in cellular inorganic phosphorus and creatine phosphate displayed a significant correlation with serum phosphorus levels. Mitochondrial respiration was impaired early in PD. Total cellular, mitochondrial, and myofibrillar creatine kinase activities were significantly reduced at 4 wk of PD and fell further at 8 and 12 wk. These data show that chronic PD is associated with reduced mitochondrial capacity to produce ATP, impaired transport via the creatine phosphate shuttle, and reduced myofibrillar ability to utilize ATP. These abnormalities indicate that all steps of myocardial energetics are impaired in PD and provide the molecular basis for the altered myocardial function seen in PD.

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.

Calcium handling by sarcoplasmic reticulum of neonatal swine cardiac myocytes

1997 ◽  
Vol 273 (1) ◽  
pp. H192-H199
Author(s):  
C. M. Hohl ◽  
B. Livingston ◽  
J. Hensley ◽  
R. A. Altschuld
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Ventricular Myocytes ◽  
Heart Function ◽  
Binding Capacity ◽  
Calcium Handling ◽  
Maximal Effect ◽  
Binding Studies ◽  
Human Infants ◽  
Cardiac Sarcoplasmic Reticulum ◽  
Length Changes

In recent years, because of similarities to human infants, neonatal piglets have increasingly become the model of choice for studying neonatal heart function. However, the cardiac sarcoplasmic reticulum (SR) has not been thoroughly characterized in this species. Accordingly, Ca2+ pump kinetics, efflux channel characteristics, Ca2+ transients, and contractile movements were examined in isolated newborn piglet cardiac ventricular myocytes. Maximum uptake rate (Vmax) and concentration required to produce a half-maximal effect (K0.5) for oxalate-supported, ATP-dependent 45Ca2+ uptake by the SR of digitonin-lysed myocytes were 285 +/- 17 nmol 45Ca2+.min-1.mg-1 and 0.69 +/- 0.07 microM, respectively. In the absence of phospholamban phosphorylation, Vmax was reduced to 195 +/- 26 nmol 45Ca2+.min-1.mg-1 (P < 0.05 vs. control) and K0.5 increased to 1.28 +/- 0.13 microM (P < 0.05 vs. control). [3H]ryanodine binding studies yielded a maximum binding capacity of 181 +/- 12 fmol/mg and a dissociation constant of 1.7 +/- 0.2 nM. Raising extracellular Ca2+ (0.5-5 mM) increased peak amplitude and decreased the duration of electrically stimulated fura 2 Ca2+ transients and recordings of cell length changes. Both ryanodine and 2,5-di-tert-butylhydroquinone, an inhibitor of SR calcium adenosinetriphosphatase, completely abolished Ca2+ transients in piglet myocytes. These studies indicate that the SR has a significant role in excitation-contraction coupling in neonatal piglet myocytes.

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 effects of vitamin E deficiency on the total fatty acids and the phospholipid fatty acids of rat tissues

1969 ◽  
Vol 23 (2) ◽  
pp. 289-295 ◽  
Author(s):  
D. J. W. Lee ◽  
M. McC. Barnes
Keyword(s):  
Fatty Acids ◽  
Vitamin E ◽  
Total Phospholipid ◽  
Rat Tissues ◽  
Vitamin E Deficiency ◽  
Deficient Diet ◽  
Acid Deficiency ◽  
Total Fatty Acids ◽  
Fatty Acid Deficiency ◽  
Kidney Liver

1. A vitamin E-low diet containing 7% stripped lard was given to hooded rats for periods up to 14 months. Control rats were given the same diet with a vitamin E supplement (I i.u./rat per day).2. No consistent pattern of changes was found in the total fatty acids of testis, lung, spleen, pancreas, heart, kidney, liver, brain, skeletal muscle and small intestine from rats given the deficient diet for 5, 6 or 7 months when compared with control rats.3. The fatty acids of the total phospholipid from the same tissues were examined after 4, 5, 8 or 14 months. In the rats deficient in vitamin E the polyunsaturated fatty acids of the linoleic series (ω6) decreased, except for 20:4ω6, which in some tissues tended to increase. After 14 months there were considerable decreases in the percentages of all the ω6 series including 20:4ω6 with increases in the percentages of 18:1ω9 and 20:3ω9 the pattern was similar to that found in essential fatty acid deficiency.

Depression of serotonin clearance by rat lungs during oxygen exposure

1977 ◽  
Vol 42 (1) ◽  
pp. 33-38 ◽  
Author(s):  
E. R. Block ◽  
A. B. Fisher
Keyword(s):  
Vitamin E ◽  
Normal Diet ◽  
Sprague Dawley ◽  
Progressive Reduction ◽  
Solution Ph ◽  
Vitamin E Deficiency ◽  
Sprague Dawley Rats ◽  
Lung Endothelium ◽  
Effect Of Oxygen ◽  
Early Alteration

The effect of oxygen (O2) exposure on the ability of the isolated, perfused rat lung to clear serotonin (5-hydroxytryptamine, 5-HT) from the perfusate was evaluated in normal or vitamin E-deficient Sprague-Dawley rats. Rats were exposed to 100% O2 at 1 ATA for 4–48 h. Lungs were subsequently isolated, artificially ventilated, and perfused in a recirculating system with Krebs-Ringer bicarbonate solution, pH 7.4 containing 3% bovine serum albumin and 0.25 muM [14C] 5-HT. 5HT clearance was calculated from the disappearance rate of [ 14C] 5-HT from the perfusate. In normal rats exposed to 100% O2, there was a progressive reduction in the clearance of 5-HT with increasing duration of O2 exposure. Compared to lungs from air-exposed controls, clearance was depressed 20% (P less than 0.01) after 18 h, 22% (P less than 0.01) after 24 h, and 35% (P less than 0.001) after 48 h. With vitamin E-deficient rats, the reduction in 5-HT clearance occurred after a shorter exposure time and was of greater magnitude than in rats on a normal diet. Depression of 5HT clearance by the lungs is an early alteration of lung function fue to hyperoxia and is potentiated by vitamin E deficiency. The most likely mechanism for the depression of 5-HT clearance is interference with the transport properties of lung endothelium.

scholarly journals Effects on Neural Function of Repleting Vitamin E–Deficient Rats With α-Tocopherol

2006 ◽  
Vol 95 (4) ◽  
pp. 2553-2559 ◽  
Author(s):  
Samantha M. Hayton ◽  
Tony Kriss ◽  
Angie Wade ◽  
David P. R. Muller
Keyword(s):  
Vitamin E ◽  
Visual Function ◽  
Human Subjects ◽  
Objective Measure ◽  
Signs And Symptoms ◽  
Tocopheryl Acetate ◽  
Neural Function ◽  
Vitamin E Deficiency ◽  
Deficient Diet ◽  
Objective Improvement

A severe and chronic deficiency of vitamin E (α-tocopherol) is associated with a characteristic neurological syndrome with typical “clinical,” neuropathological, and electrophysiological abnormalities in both humans and experimental animals. Repletion of vitamin E–deficient human subjects with α-tocopherol typically halts the progression of the neural signs and symptoms, and in some cases, can result in objective improvement. Electrophysiological parameters provide an objective measure of neural and visual function and improvement of some of these measures has been reported after repletion with vitamin E in humans. In this longitudinal study, the effects of repleting rats with a diet containing 36 mg/kg all-rac-α-tocopheryl acetate for 20 wk after they had been receiving a vitamin E–deficient diet for 38 wk was studied. We report significant improvements in growth and a number of electrophysiological parameters of both neural and visual function after repletion. These results confirm the validity of the vitamin E–deficient rat as a model of vitamin E deficiency in humans.

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