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

Abstract

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.

Modification of Epinephrine-induced Arrhythmias by N-Acetyl-L-Cysteine and Vitamin E

“…In both pretreated animal groups, the level of oxidation products of catecholamines was significantly decreased, whereas the plasma levels for both epinephrine and norepinephrine were unaffected. Because the oxidized catecholamines are known to induce alterations in cation homeostasis as well as energy production, 5,6,8 and vitamin E has been reported to attenuate these disturbances, 18,20,39 it appears that similar mechanisms could, at least partially, account for the improvement of catecholamine-induced arrhythmias. However, the effects of antioxidants on other sites such as b 1 -adrenoreceptors and adenylyl cyclase 40 may also explain the antiarrhythmic actions of vitamin E and NAC.…”

“…16,17 The beneficial effects of a well-known antioxidant, vitamin E, in preventing disturbances in energy metabolism, changes in membrane permeability, and Ca 2þ handling defects in the heart induced by a synthetic catecholamine, isoproterenol, have been reported in previous studies. [18][19][20] Likewise, vitamin E was found to reduce the incidence of premature ventricular contractions (PVCs), infarct size, and mortality due to coronary artery ligation. 21 However, very little information regarding the influence of vitamin E on the genesis of epinephrine-induced arrhythmias is available in the literature.…”

Effectiveness of Some Vitamins in the Prevention of Cardiovascular Disease: A Narrative Review

“…Rabbits fed on vitamin E deficient diet showed several electrocardiographic abnormalities; these alterations in the heart were accompanied by a reduction in high energy phosphate and glycogen stores (Mulder et al, 1954). Heart failure associated with marked metabolic changes were also seen in animals maintained on vitamin E deficient diet (Lu et al, 1941;Gullickson and Calverley, 1946;Draper et al, 1952;Fedelesova et al, 1971). In addition, marked alterations in SL Na + -K + ATPase and sarcoplasmic reticular (SR) Ca 2+ -pump ATPase as well as SR Ca 2+ -uptake and Ca 2+ -release activities were decreased in vitamin E deficient rat heart (Fedelesova et al, 1971).…”

“…Heart failure associated with marked metabolic changes were also seen in animals maintained on vitamin E deficient diet (Lu et al, 1941;Gullickson and Calverley, 1946;Draper et al, 1952;Fedelesova et al, 1971). In addition, marked alterations in SL Na + -K + ATPase and sarcoplasmic reticular (SR) Ca 2+ -pump ATPase as well as SR Ca 2+ -uptake and Ca 2+ -release activities were decreased in vitamin E deficient rat heart (Fedelesova et al, 1971). It should be mentioned that cardiac abnormalities due to vitamin E deficiency were accompanied by muscular dystrophy (Grigoreva and Medovar, 1959;Read and Nehorayan, 1959;Dhalla et al, 1971;Fedelesova et al, 1971).…”

A Mechanism of the Acceleration of Lipid Peroxide Formation in Liver Homogenates and Subcellular Fractions of Vitamin E-Deficient Mice

“…However, it would matter little to the acceleration in vitamin E deficiency because the lipid peroxidation in normal liver homogenate was little affected even though ascorbate, NADH or NADPH was added (Table 5). Further, it has been described that no significant differences exist either in lipid peroxidizing activity of soluble fraction or in contents of ascorbate between E-deficient animal and normal control (56,57), and NADP and NADPH contents showed rather large decreases in E deficiency (58). Phenobarbital treatment accelerated both drug metabolization and lipid peroxidation which involved several common steps, while tocopherol deficient or in vitro addition of Tween 80 resulted in decrease of oxidation of aminopyrine along conversely with increase of lipid peroxidation (Table 7).…”