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PubMed1981

Effects of diabetes and fasting on pantothenic acid metabolism in rats.

The effects of fasting and diabetes on pantothenic acid (PA) metabolism were studied in rats. Tissue levels of PA and coenzyme A (CoA) and rates of [14C]PA uptake and incorporation into tissue CoA were determined. Both fasting and diabetes resulted in accelerated rates of [14C]PA uptake, higher tissue concentrations of PA, increased incorporation of [14C]PA into CoA, and elevated tissue concentrations of CoA in the liver. The concentration of PA in liver was near the Km of pantothenate kinase for PA in control animals, and increased PA uptake may, in part, account for the increased [14C]PA incorporation into CoA though an elevation in tissue PA levels. In cardiac muscle, increased [14C]PA incorporation into CoA and increased CoA levels were associated with reduced PA uptake and reduced tissue PA levels in both fasting and diabetic animals, suggesting that CoA synthesis is not controlled by substrate availability in this tissue. Uptake of [14C]PA by skeletal muscle was also reduced in diabetic animals. These data suggest that PA uptake by tissues is under metabolic or hormonal control. Decreased uptake by muscle and increased uptake by liver may represent a mechanism for shifting large body stores of PA present in muscle to the liver in which endogenous PA concentrations are normally low. In addition, both fasting and diabetes resulted in decreased urinary PA excretion, a finding that may represent a regulatory mechanism to conserve whole-body PA under these conditions.

Animals↗
PubMedDate not supplied

Determination of pantothenic acid in foods by optical biosensor immunoassay.

An optical biosensor inhibition immunoassay was developed using a specific pantothenic acid-binding protein for the quantitation of free pantothenic acid (vitamin B5) in foodstuffs. Samples were prepared by a simple extraction procedure in buffer, and vitamin content was estimated against authentic calibrants in the same buffer. Performance parameters included a working range of 10-5000 ng/mL, a limit of detection of 4.4 ng/mL, precision relative standard deviation of 5.4-7.1% over a range of concentrations, and recoveries > 95% in the matrixes tested. A wide range of foodstuffs, including National Institute of Standards and Technology reference samples, were tested in 3 independent laboratories and the results were compared with microbiological assay and liquid chromatography/mass spectrometry (LC/MS) methods. The results indicate that the biosensor technique is appropriate for the estimation of pantothenic acid in a wide range of foodstuffs.

Biosensing Techniques↗
PubMed1996

Noxious effects of oxygen reactive species on energy-coupling processes in Ehrlich ascites tumor mitochondria and the protection by pantothenic acid.

Irradiation of Ehrlich ascites tumor cells with ultraviolet light or exposure to the Fenton reaction results in lesions in the mitochondrial energy-coupling system. Formation of the membrane potential and its utilization for ATP synthesis are more affected than the respiratory chain. Preincubation of the cells with pantothenic acid or its derivatives which can serve as precursors of CoA largely protects against the damage of mitochondrial energetics by oxygen reactive species formed by UV light or the Fenton reaction. Incubation of Ehrlich ascites tumor cells with pantothenic acid increases their content of glutathione (most of which is present in the reduced form) by 40%. It is concluded that the protective effect of precursors of CoA against lesions of the mitochondrial energy-coupling system by oxygen reactive species is mainly due to removal of free radicals and peroxides by glutathione peroxidase and phospholipid hydroperoxide glutathione peroxidase.

Animals↗
PubMedDate not supplied

Effects of pantethine, cysteamine and pantothenic acid on open-field behavior and brain catecholamines in rats.

Cysteamine (1.95 mM/kg) markedly decreased the locomotor, rearing and grooming activities, as well as the number of defecation boluses in an open-field test. An equimolar dose of pantethine reduced the locomotor activity to a lesser extent, but has the same potency in decreasing the number of defecation boluses, whereas pantothenic acid did not affect the behavior of the rats. Cysteamine, and to a lesser extent pantethine, reduced the noradrenaline and increased the dopamine and DOPAC concentrations in the hypothalamus. Pantothenic acid itself did not influence the hypothalamic catecholamine concentrations. These results suggest that the lower efficacy of pantethine compared to cysteamine on both behavioral and neurochemical parameters is probably due to a rate-limiting activity of the enzyme pantetheinase in the conversion of pantetheine to cysteamine.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1976

Nutritional status of pantothenic acid in Indian pregnant and nursing women.

Investigations on nutritional status of pantothenic acid were carried out in 57 pregnant women and 24 lactating mothers belonging to the low socio-economic group. Fourteen non-pregnant, non-lactating women from the same group served as controls. Pregnant subjects had blood levels of the vitamin comparable to those of the control group while cord blood contained significantly higher concentrations of patnothenic acid than did the maternal blood. The urinary excretion of the vitamin in pregnant women was comparable to that in the control group. Blood and milk levels of the vitamin in the nursing women were in the reported range.

Erythrocytes↗
PubMed1983

Dietary pantothenic acid requirement of fingerling channel catfish.

Two experiments were conducted to reevaluate the dietary pantothenic acid requirement for fingerling channel catfish. Purified diets supplemented with calcium d-pantothenate were used in both experiments. The results indicate that the previously reported requirement value was underestimated. The minimum dietary calcium d-pantothenate level that produced maximum growth, feed efficiency and prevented the characteristic deficiency sign of gill lesions was 15 mg/kg of diet. The gill lesions were detected in 2 weeks in fish fed deficient diets. A reduction in the gill lesions was evident within 2 weeks after fish fed the deficient diet were converted to a diet containing 40 mg calcium d-pantothenate per kilogram of diet. In one experiment there appeared to be a high correlation between disease susceptibility and dietary calcium d-pantothenate level. Based on these observations and since the requirement may vary depending on fish size, age, water temperature, water ionic strength, fish density, oxygen availability, etc., we recommend a value of 30 mg calcium d-pantothenate per kilogram of diet be used in formulating catfish feeds.

Animal Nutritional Physiological Phenomena↗
PubMedDate not supplied

[Therapeutic efficacy of pantothenic acid preparations in ischemic heart disease patients].

The therapeutic effectiveness of the pantothenic acid drugs: calciipantothenas and pantethine, was studied in 182 patients with coronary heart disease and stable angina of effort. It is shown that both the drugs produce favourable effects on certain parameters of hemodynamics, on the metabolism of lipids, riboflavin and ascorbic acid. It is recommended that the administration of calciipantothenas in a dose of 300 mg/day, during 3 weeks, be included into the combined treatment of coronary patients with no manifest disorders of lipid metabolism. Patients with manifest hyperlipidemia should be administered pantethine in a dose of 500 mg/day.

Adult↗
PubMed1991

Reassessment of pantothenic acid requirement for single comb White Leghorn pullets from 0 to 6 weeks of age and its subsequent effect on sexual maturity.

Two experiments were conducted using a total of 288 Hy-Line W-36 day-old pullets in each experiment. The pullets were randomly assigned to one of the six dietary treatments that consisted 0, .3, .6, .9, 1.8, or 3.6 mg supplemental pantothenic acid/kg of a corn and soybean meal basal diet (4.8 mg/kg). Six replicates of eight pullets per replicate were used per treatment in each experiment. Feed and water were provided for ad libitum access. The pullets were housed in battery brooder pens with raised wire floors. Body weight, body weight gain, average feed consumption per day, total feed consumption, and feed conversion were determined at 3 and 6 wk of age (WOA). The birds were observed for any signs of pantothenic acid deficiency. At the end of a 6-wk experimental period, the pullets previously receiving the diets containing either 0 or 3.6 mg supplemental pantothenic acid/kg of diet were raised to sexual maturity and their age at sexual maturity, body weight at 24 WOA, and average number of eggs per pullet through 32 WOA were measured in both of the experiments. No differences (P greater than .05) in total body weight, body weight gain, average feed consumption per day, total feed consumption, and feed conversion were observed in any of the supplemental pantothenic acid treatments from 0 to 3 and 3 to 6 WOA. None of birds during the experimental period showed any signs of deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Effect of pantothenic acid status on the content of the vitamin in human milk.

Seventeen lactating women who delivered preterm infants (between 28 to 34 wk of gestational age) and 26 nursing mothers of term infants participated in the study. Each term mother kept a record of 2-day dietary intakes, collected urines for 2 days, and provided fore and hind milk samples and a fasting blood sample at 2 and 12 wk postpartum. Each of preterm women provided fore and hind milk samples once a week for 16 wk starting 2 wk postpartum. The method of determining pantothenic acid content in milk samples was validated, and the vitamin was quantitated by the radioimmunoassay. The average pantothenate levels in fore and hind samples of preterm milk (3.31 and 3.72 micrograms/ml, respectively) were significantly (p less than 0.05) higher than those of term milk (2.64 and 2.48 micrograms/ml, respectively). No significant change was observed in pantothenic acid content within a feeding or with the progress of nursing in both groups. The vitamin content of human milk was compared with the minimum requirement of the Infant Formula Act of 1980. The pantothenate level in term milk was significantly (p less than 0.05) correlated with the vitamin level in maternal circulation and with that of the dietary intake and urinary excretion.

Adult↗
PubMed1995

Pantothenic acid deficiency as the pathogenesis of acne vulgaris.

For years, the pathogenesis of acne vulgaris has been known to be strongly influenced by hormonal factors. However, the exact role of and the interrelationship among the various hormones in question have not been well elucidated. Here, I wish to suggest a radically different theory for its pathogenesis and relate its basic pathology to a deficiency in pantothenic acid, a vitamin hitherto not known to cause any deficiency syndrome in humans. Hence, the effect of hormonal factors in this disease entity becomes secondary to that of the availability of pantothenic acid. A complete cure of this condition is effected by a very liberal replacement therapy with the vitamin.

Acne Vulgaris↗
PubMed1992

Effect of pantothenic acid on disposition kinetics and tissue residues of sulphadimidine in chickens.

Sulphadimidine was administered to chickens via the intracrop route to determine plasma concentrations of the unchanged sulphonamide and its acetylated derivatives, kinetic disposition, tissue residues and acetylation. The sulphadimidine was given alone (group 1) at a dose of 200 mg kg-1 bodyweight. Pantothenic acid was given via the intracrop route at a dose of 100 mg kg-1 bodyweight one hour before (group 2) and six hours after (group 3) sulphadimidine administration (200 mg kg-1 bodyweight intracrop). The highest plasma concentrations of sulphadimidine in groups 1, 2 and 3 were reached in 1.73, 1.62 and 1.71 hours, respectively, following intracrop administration. In birds of groups 1, 2 and 3 no sulphadimidine was detected at 72, 24 and 48 hours, respectively, following its administration. Estimation of sulphadimidine in most of the body tissues revealed that all tissues examined had lower concentrations than plasma. In chickens given pantothenic acid (groups 2 and 3) before and after sulphadimidine administration, an increase in the concentration of N4 acetylated derivatives of sulphadimidine was observed compared with birds given sulphadimidine alone (group 1).

Animals↗
PubMed1988

Identification of [1-14C]pantothenic-acid-mediated modified mitochondrial proteins.

The in vivo administration of [1-14C]pantothenic acid, which is the precursor of coenzyme A, resulted in the radioactive labelling of several mitochondrial proteins in rat liver. The incorporated radioactivity could be released by glutathione or 2-mercaptoethanol. Two mitochondrial matrix proteins acetyl-CoA acetyltransferase (liver and heart), an enzyme involved in the biosynthesis or degradation of ketone bodies, and 3-oxoacyl-CoA thiolase (liver), a protein participating in fatty acid oxidation were identified as modified proteins. The radioactivity was localized exclusively in forms A1 and A2 indicating that these forms represent the modified states of the acetyl-CoA acetyltransferase protein. Kinetics of incorporation of radioactivity revealed an accumulation of the modified forms. The ratio of specific radioactivities of A2 compared to A1 was 2.41 +/- 0.15 (n = 10). After in vivo labelling with [14C]leucine, the specific radioactivity of acetyl-CoA acetyltransferase depended on the state of the enzyme protein. The unmodified enzyme exhibited a lower specific radioactivity than its modified forms suggesting different turnover rates of these proteins.

Acetyl-CoA C-Acetyltransferase↗
PubMed1995

Pantothenic acid decreases valproic acid-induced neural tube defects in mice (I).

The effect of the administration of pantothenic acid (PTA) on valproic acid (VPA)-induced teratogenesis was examined in ICR mice. VPA (300, 400, and 500 mg/kg, s.c.) or PTA (3 x 10, 3 x 100, and 3 x 300 mg/kg, i.p.) was injected on day 8.5 of gestation (plug day = day 0.5). Exencephaly was induced dose dependently by single injections of VPA. Three administrations of PTA alone at any dose levels showed neither embryocidal nor teratogenic effects. In combined treatment experiments, PTA (3 x 300 mg/kg) was injected 1 hr before, immediately before, and 1 hr after VPA administration. PTA significantly reduced VPA-induced exencephaly, while none of the other external malformations such as open eyelid or skeletal malformations such as fused, absent, or bifurcated ribs and fused thoracic vertebrae and fused sternebrae were reduced. The results suggest that PTA reduces the incidence of neural tube defect induced by VPA in mice.

Abnormalities, Drug-Induced↗
PubMed1986

Pantothenic acid transport and metabolism in the central nervous system.

The mechanisms by which pantothenic acid (PA) enters and leaves brain, choroid plexus, and cerebrospinal fluid (CSF) were investigated by injecting [3H]PA either intravenously or intraventricularly into adult rabbits. [3H]PA, either alone or together with unlabeled PA, was infused at a constant rate into conscious rabbits. At 180 min, [3H]PA readily entered CSF, choroid plexus, and brain. In brain, CSF, and plasma, greater than 90% of the 3H was associated with [3H]PA. The addition of 200 mumol/kg PA to the infusion syringe decreased the penetration of [3H]PA into brain and CSF by approximately 70%. Two hours after the intraventricular injection of [3H]PA, [3H]PA was rapidly cleared from the CSF by a probenecid-sensitive mechanism. No metabolism of the [3H]PA occurred in brain. However, 18 h after the intraventricular injection of 37 microCi (34 nmol) of [3H]PA, approximately 40% of the 3H remaining in forebrain was converted to [3H]CoA. These results show that PA enters and leaves CSF and brain by saturable transport systems. However, [3H]PA is very slowly converted to [3H]CoA in brain in vivo.

Animals↗
PubMed1994

Dilated cardiomyopathy due to type II X-linked 3-methylglutaconic aciduria: successful treatment with pantothenic acid.

A case of dilated cardiomyopathy in a young boy secondary to type II 3-methylglutaconic aciduria is described. A metabolic cause for his dilated cardiomyopathy was suspected because of the development on the electrocardiogram of an unusual "camel's hump" shape of the T waves, and of progressive thickening with increasing echogenicity of the left ventricular wall. He initially improved on digoxin treatment, but did not maintain the response with conventional dietary treatment for this condition. Supplementation with L-carnitine was associated with rapid deterioration in cardiac state, and may be contraindicated in this condition. At a point when the patient was moribund, large doses of pantothenic acid, a precursor of coenzyme A, produced a dramatic and sustained improvement in myocardial function and in growth, neutrophil cell count, hypocholesterolaemia, and hyperuricaemia, which suggests that limitation of availability of coenzyme A is a fundamental pathological process in this condition. The clinical improvement has been maintained for 13 months, and myocardial function is now nearly normal. Oral pantothenol, unlike pantothenic acid, is not efficacious.

Amino Acid Metabolism, Inborn Errors↗