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Results for “PANTOTHENIC ACID”

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PubMed1995

Pantothenic acid and its derivatives protect Ehrlich ascites tumor cells against lipid peroxidation.

Preincubation of Ehrlich ascites tumor cells at 22 or 32 degrees C, but not at 0 degree C, with pantothenic acid, 4'-phosphopantothenic acid, pantothenol, or pantethine reduced lipid peroxidation (measured by production of thiobarbituric acid-reactive compounds) induced by the Fenton reaction (Fe2+ + H2O2) and partly protected the plasma membrane against the leakiness to cytoplasmic proteins produced by the same reagent. Pantothenic acid and its derivatives did not inhibit (Fe2+ + H2O2)-induced peroxidation of phospholipid multilamellar vesicles, thus indicating that their effect on the cells was not due to the scavenging mechanism. Homopantothenic acid and its 4'-phosphate ester (which are not precursors of CoA) neither protected Ehrlich ascites tumor cells against lipid peroxidation nor prevented plasma membrane leakiness under the same conditions. Incubation of the cells with pantothenic acid, 4'-phosphopantothenic acid, pantothenol, or pantethine significantly increased the amount of cellular CoA and potentiated incorporation of added palmitate into phospholipids and cholesterol esters. It is concluded that pantothenic acid and its related compounds protect the plasma membrane of Ehrlich ascites tumor cells against the damage by oxygen free radicals due to increasing cellular level of CoA. The latter compound may act by diminishing propagation of lipid peroxidation and promoting repair mechanisms, mainly the synthesis of phospholipids.

Animals↗
PubMed1976

Measurements of urinary pantothenic acid excretions of alcoholic patients.

Malnutrition is often associated with alcoholism. Nutritional deficiencies found in alcoholic patients are mostly related to protein and B-vitamins. The purpose of this study was to determine whether pantothenic acid nutrition is altered in patients with prolonged intake of alcohol. Urinary pantothenic acid was measured in alcoholic patients during three intervals in a 10-week rehabilitation period. Pantothenic acid excretion of alcoholic patients revealed a lower excretion in an acute phase of the disease (2.7 mg/day) than reported excretion of normal individuals (3.9 mg/day). Inadequate intake of nutrients may have been a contributing factor. In chronic alcoholic patients who participated in a 10-week rehabilitation program, excretion approximated intake at the beginning of the period (6.6 mg/day) and decreased to less than one-half this amount (2.7 mg/day) at the end of the rehabilitation. It may be speculated that alcoholic patients, in general, are unable to utilize pantothenic acid from the diet efficiently, but as they are rehabilitated, more of this vitamin is retained in the body for useful functions.

Adult↗
PubMedDate not supplied

[Pantothenic acid biotransformation in human vitamin deficiency].

Content of CoA and pantothenic acid in leukocytes as well as excretion of the vitamin derivatives, estimated by microbiological procedure, with urine with 6 and 24 hrs after administration per os or intramuscularly of 200 mg calcium pantothenate were studied in 42 donors and 25 patients with chronic alcoholism. In all the cases content of CoA of the pantothenate metabolites were increased in leukocytes within 6 hrs after the vitamin loading. Excretion of pantothenic acid and its derivatives with urine was increased for a short time in healthy persons after loading, however its total content maintained similar to normal values within 24 hrs. In the patients with chronic alcoholism the increase in concentrations of the components studied in leukocytes was accompanied by a distinct increase in excretion of the vitamin with urine within 24 hrs.

Adult↗
PubMed1991

Acute encephalopathy with hepatic steatosis induced by pantothenic acid antagonist, calcium hopantenate, in dogs.

In Japan, acute encephalopathy with hepatic steatosis resembling Reye's syndrome has been reported to occur after treatment with the pantothenic acid antagonist, calcium hopantenate. We studied the causal relationship and the pathogenesis in dogs. The agent was administered to seven dogs at increasing doses over a period of 8 weeks. Anorexia, vomiting, and diarrhea were common clinical findings. In four dogs, coma suddenly developed after the appearance of gastrointestinal signs. Three animals died during periods when they were not under direct observation. The effects of the agent appear to be related to dose. Laboratory findings representing significant changes at the time of coma included hypoglycemia, leukocytosis, hyperammonemia, hyperlactatemia, and elevated levels of serum transaminases. Microvesicular hepatic steatosis and mitochondrial abnormalities were consistent pathological findings. The hepatic mitochondria were enlarged and characterized by an increased number of cristae and the presence of crystalloid inclusions. In a second group of four dogs, pantothenic acid was given in addition to and in the same amount as calcium hopantenate at increasing doses over a period of 8 weeks. All four dogs survived the 8 weeks and only one developed mild anorexia. No significant biochemical changes were found and neither hepatic steatosis nor mitochondrial abnormalities were observed. The addition of pantothenic acid prevented the development of the disorder in the four animals. These results show that calcium hopantenate produces acute encephalopathy with hepatic steatosis in dogs, by inducing a deficiency of pantothenic acid. The hepatic mitochondrial changes of this reaction differ from those of Reye's syndrome.

Acute Disease↗
PubMed1995

[B-vitamins (thiamine, vitamin b6, pantothenic acid) in lean muscle tissue of growing cattle of the German Simmental breed under different feeding intensities].

In a comparative slaughter experiment the thiamin, vitamin B6 and pantothenic acid content of lean tissue of foreloin of growing cattle was determined by whole body analyses. 54 bulls, 45 heifers and 45 steers were fed until a live mass of 200 kg, 350 kg, 425 kg (only heifers) 500 kg and 575 kg, 650 kg, respectively (only bulls and steers). One half of each carcass was divided into 13 cuts and afterwards the cuts were each divided into lean, adipose and bone tissue and tendons. The lean tissue of the foreloin was subjected to analysis of thiamin, vitamin B6 and pantothenic acid. The mean thiamin content of 0.75 mg kg-1 fresh matter (200 kg live mass) decreased with rising live mass and under intensive feeding conditions in bulls and steers to 0.53 mg and in heifers to 0.61 mg. Restrictively feeding caused a mean thiamin content of 0.60 mg per kg fresh matter in bulls, steers and heifers. Under both feeding conditions in the lean tissue of the foreloin on average a vitamin B6 content of 2.6 mg (bulls), 3.1 mg (heifers) and 3.0 mg kg-1 fresh matter (steers) was analysed. A mean content of pantothenic acid of 2.6 mg kg-1 fresh matter was determined in bulls independent of live mass and feeding intensity. In heifers the content of pantothenic acid on average was 3.0 mg under intensive feeding system and 2.6 mg under low feeding conditions, whereas steers reached contents of 2.7 mg (high feeding) and 2.2 mg kg-1 fresh matter (low feeding).

Animal Feed↗
PubMed1993

[Pantothenic acid levels in blood of athletes at rest and after aerobic exercise].

Ninety-six high-performance athletes of various disciplines were available for this investigation. All athletes had many years of training and competition experience. The pantothenic acid contents in the blood were determined by means of microbiological measurements. In addition to the pantothenic acid level at rest, measurements were made resp. physical exertion in 14 marathon runners and nine body builders. Blood was collected for determination of pantothenic acid before (a), after (b) and 2 h after exercise. Compared to the reference values for untrained persons (1.34 +/- 0.13 nmol/mL), the marathon runners with 0.76 (0.31-0.94) nmol/mL and soccer players with 1.19 (0.37-2.64) nmol/mL were below the reference values. According to relative frequencies, more than 30% of all athletes were below the lower limit (< 1.20 nmol/mL). The values in body builders/racing cyclists differed significantly from those in marathon racers (p < 0.001), which is presumably due to unallowed supplementation. During exercise, there was a significant increase in the pantothenic acid level in marathon runners (p < 0.01).

Adult↗
PubMed1983

[Pantothenic acid metabolic disorder and its relation to the change in energy processes in patients with ischemic heart disease and hypertension].

Pantothenic acid metabolism and the status of energy processes in leukocytes were examined in 171 patients with hypertension and coronary heart disease. It was shown that the patients' body supply with the vitamin decreased as the disease progressed and heart failure supervened. The deficiency of pantothenic acid was shown to be interrelated with the impairment of energy processes. Application of pantothenate in a dose of 200 mg a day for two weeks led to the increased content of pantothenic acid and to normalization of energy processes.

Aged↗
PubMed1981

Pantothenic acid content of 75 processed and cooked foods.

Seventy-five foods in a ready-to-eat state were analyzed for pantothenic acid using a new radioimmunoassay. Meats, potatoes, oat cereals, tomato products, and whole grains were among the better sources of pantothenic acid, supplying from 2 to 9 mg. per 1,000 kcal. Fruit products and corn-based and presweetened cereals were among the poorest sources of the vitamin. Results of the study suggest a need for careful selection of foods for pantothenic acid content by individuals on a low-energy diet.

Cooking↗
PubMed1966

Liquid nitrogen preservation of Saccharomyces carlsbergensis and its use in a rapid biological assay of pantothenic acid.

A rapid direct turbidimetric determination of pantothenic acid with the use of Saccharomyces carlsbergensis was developed. With a 5.5-hr incubation, the bioassay demonstrated good dose responses within a range up to 0.04 mug/ml of calcium pantothenate. The multivitamin product assay values obtained by the rapid assay method compare well with the values obtained by the standard USP method. beta-Alanine interference was reduced to an insignificant level by the incorporation of asparagine in the assay medium. The Upjohn complex products which require Mylase-P enzyme digestion treatments were also satisfactorily assayed.

Alanine↗
PubMed1995

Effect of pantothenic acid and ascorbic acid supplementation on human skin wound healing process. A double-blind, prospective and randomized trial.

This study aimed at testing human skin wound healing improvement by a 21-day supplementation of 1.0 g ascorbic acid (AA) and 0.2 g pantothenic acid (PA). 49 patients undergoing surgery for tattoos, by the successive resections procedure, entered a double-blind, prospective and randomized study. Tests performed on both skin and scars determined: hydroxyproline concentrations, number of fibroblasts, trace element contents and mechanical properties. In the 18 supplemented patients, it was shown that in skin (day 8) Fe increased (p < 0.05) and Mn decreased (p < 0.05); in scars (day 21), Cu (p = 0.07) and Mn (p < 0.01) decreased, and Mg (p < 0.05) increased; the mechanical properties of scars in group A were significantly correlated to their contents in Fe, Cu and Zn, whereas no correlation was shown in group B. In blood, AA increased after surgery with supplementation, whereas it decreased in controls. Although no major improvement of the would healing process could be documented in this study, our results suggest that the benefit of AA and PA supplementation could be due to the variations of the trace elements, as they are correlated to mechanical properties of the scars.

Adolescent↗
PubMed1996

Determination of pantothenic acid in infant milk formulas by high performance liquid chromatography.

A reverse-phase liquid chromatographic method was adapted for the assay of pantothenic acid in infant milk formulas. Sample preparation consisted of deproteination with acetic acid and sodium acetate solutions, followed by centrifugation and filtration. The chromatographic system included a C-18 column and a mobile phase consisting of a sodium phosphate buffer and acetonitrile (97:3, vol/vol). The column effluent was monitored by UV detection at 197 nm. The system was linear from 50 to 800 ng. The recoveries of pantothenic acid from augmented samples ranged from 89 to 98%, and the coefficients of variation ranged from 1.17 to 3.20%. The results obtained with the HPLC and a microbiological method were highly correlated for starting infant formula, follow-up infant formula, and formula for infants of low birth weight from four different manufactures. All formulas analyzed contained pantothenic acid at concentrations higher than those declared on their nutritional labels and were in compliance with international recommendations.

Chromatography, High Pressure Liquid↗
PubMed1988

Reye-like syndrome following treatment with the pantothenic acid antagonist, calcium hopantenate.

Three senile patients developed fatal acute encephalopathy while receiving calcium hopantenate. The clinical, biochemical, and pathological picture was similar to Reye's syndrome. Calcium hopantenate is a pantothenic acid antagonist. The serum levels of calcium hopantenate were high in coma, and that of pantothenic acid examined in one patient was lowered. Evidence obtained indicated that the Reye-like syndrome might be caused by calcium hopantenate possibly due to the induction of pantothenic acid deficiency.

Aged↗