EFFECTS OF DIETARY LEVELS OF MACRONUTRIENTS ON VITAMIN REQUIREMENTS.
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Ascorbic Acid↗
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[THE VITAMIN REQUIREMENTS OF THERMOPHILIC BACTERIA].
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Bacillus↗
Role of pantothenic and ascorbic acid in wound healing processes: in vitro study on fibroblasts.
In order to analyze the possible role of pantothenic acid (PA) and ascorbic acid (AA) in wound healing processes, the effects of these vitamins upon the growth of fibroblasts, obtained from human fetal skin or foreskin, were studied. Cell proliferation, protein synthesis and protein release were evaluated. The rate of cell growth remained identical when PA or AA were added to the culture medium. PA increased the basal incorporation of 14C proline into precipitated material while AA did not modify this action. However, when cultures were incubated with PA and AA, the release of intracellular protein into the culture medium increased. These results suggest that the combined use of these two vitamins might be of interest in postsurgical therapy and in wound healing.
Ascorbic Acid↗
Identification and characterization of the main beta-alanine uptake system in Escherichia coli.
In Escherichia coli, beta-alanine is a direct precursor in the biosynthesis of pantothenic acid (vitamin B5). Although a sufficient beta-alanine supply is crucial for biotechnological vitamin B5 production, nothing was known about beta-alanine transport in E. coli until now. The aim of this work was the characterization of beta-alanine transport by E. coli and the identification and overexpression of the corresponding carrier-encoding gene for the rational improvement of pantothenic acid-producing strains. beta-Alanine uptake was found to be an active process catalyzed by the amino acid carrier CycA. The corresponding gene was cloned and overexpressed, resulting in an increase in the uptake rate, compared with the wild type. In all tested strains, this overexpression led to a strong sensitivity to beta-alanine, but not to the other CycA substrates, such as L-alanine, D-alanine, and glycine. This prevented a direct application for the improvement of pantothenic acid-producing strains by an enhanced precursor supply.
Alanine↗
Protection by pantothenol and beta-carotene against liver damage produced by low-dose gamma radiation.
Rats were exposed to a total dose of 0.75 Gy of gamma radiation from a 60Co source, receiving three doses of 0.25 Gy at weekly intervals. During two days before each irradiation, the animals received daily intragastric doses of 26 mg pantothenol or 15 mg beta-carotene per kg body mass. The animals were killed after the third irradiation session, and their blood and livers were analyzed. As found previously (Slyshenkov, V.S., Omelyanchik, S.N., Moiseenok, A.G., Trebukhina, R.V. & Wojtczak, L. (1998) Free Radical Biol. Med. 24, 894-899), in livers of animals not supplied with either pantothenol or beta-carotene and killed one hour after the irradiation, a large accumulation of lipid peroxidation products, as conjugated dienes, ketotrienes and thiobarbituric acid-reactive substances, could be observed. The contents of CoA, pantothenic acid, total phospholipids, total glutathione and GSH/GSSG ratio were considerably decreased, whereas the NAD/NADH ratio was increased. All these effects were alleviated in animals supplied with beta-carotene and were completely abolished in animals supplied with pantothenol. In the present paper, we extended our observations of irradiation effects over a period of up to 7 days after the last irradiation session. We found that most of these changes, with the exception of GSH/GSSG ratio, disappeared spontaneously, whereas supplementation with beta-carotene shortened the time required for the normalization of biochemical parameters. In addition, we found that the activities of glutathione reductase, glutathione peroxidase, catalase and NADP-dependent malate (decarboxylating) dehydrogenase ('malic enzyme') in liver were also significantly decreased one hour after irradiation but returned to the normal level within 7 days. Little or no decrease in these activities, already 1 h after the irradiation, could be seen in animals supplemented with either beta-carotene or pantothenol. It is concluded that pantothenol is an excellent radioprotective agent against low-dose gamma radiation.
Animals↗
Nutritional deficiency anemias in nonhuman primates.
The purpose of this report is to review past studies in which anemias, occurred spontaneously in nonhuman primates due to feeding inadequate diets or were induced by feeding diets deficient in a nutrient. Included is a review of anemias induced by deficiencies of iron, niacin, pyridoxine, pantothenic acid, protein, riboflavin, cyanocobalamin, folic acid, ascorbic acid and alpha-tocopherol. The anemia induced by deficiency of each nutrient is discussed with emphasis on the major clinical signs as well as peripheral blood and bone marrow pathology. Results of supplementation of the diet following induction of deficiency states are discussed also. Whenever applicable, a discussion is included of the use of nonhuman primates as animal models for studies simulating parallel nutritional deficiencies in man.
Anemia↗
[Maternal deficiencies in pantothenic and folic acid].
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Avitaminosis↗
Vitamin levels in chronic renal failure and need for supplementation.
Deficiencies of water-soluble vitamins may occur in uremic patients mainly because of restricted consumption and of loss during chronic hemo- and peritoneal dialysis. Although the daily requirement for most vitamins is not well defined in chronic renal failure supplementation of the vitamins thiamine, riboflavin, pyridoxine, pantothenic acid, niacin and ascorbic acid, the form of one multivitamin preparation without vitamin A as well as folic acid in dialysis patients after each dialysis is recommended. There is no need for vitamin B12, vitamin A and vitamin E.
Ascorbic Acid↗
Pantothenate transport in Escherichia coli.
The transport system for pantothenic acid uptake in Escherichia coli was characterized. This transport system was specific for pantothenate, had a Kt of 0.4 microM, and had a maximum velocity of 1.6 pmol/min per 10(8) cells (45 pmol/min per mg [dry weight]). Pantothenate uptake was not reduced in osmotically shocked cells or by ATP depletion with arsenate, but was reduced greater than 90% by the dissipation of the membrane electrochemical gradient with 2,4-dinitrophenol. Sodium ions stimulated pantothenate uptake (Kt, 0.8 mM) by reducing the Kt for pantothenate by an order of magnitude. Intracellular pantothenate was rapidly phosphorylated, but phosphorylation of pantothenate was not required for uptake since pantothenate was the only labeled intracellular compound concentrated by ATP-depleted, glucose-energized cells. The data were consistent with the presence of a high-affinity pantothenate permease that concentrates the vitamin by sodium cotransport.
Biological Transport↗
The permeability properties of the parasite cell membrane.
The asexual development of the malaria parasite takes place inside the host's erythrocyte, an environment that is different from that of most other eukaryotic organisms. The intense and rapid development of the parasite, as well as the homeostatic regulation of its cellular composition, require an extensive exchange of material between the parasite and its immediate surroundings. Studies on free murine parasite species suggest that a plasma membrane H+ pump is responsible for the maintenance of membrane potential and pH gradient, which are used as driving forces for the uptake of glucose and extrusion of Ca2+ by means of a symporter and an antiporter, respectively. In Plasmodium falciparum, a similar transport of Ca2+ may prevail. Several other transporters have been assigned to the plasma membrane of this parasite, either by direct measurements or by inference: D-glucose, nucleosides, L-amino acids, L-lactate and pantothenic acid. A Na+/H+ antiporter has been demonstrated, and implicated in the regulation of pH, and an ATP/ADP antiporter, whose function remains controversial, has been characterized. The presence of Mg2+ and Na+/K+ pumps and an active extrusion of oxidized glutathione can be inferred from the composition of the parasite cytosol vs. that of the host cell. Several genes coding for cation pumps have been cloned and their functions await characterization.
Amino Acid Sequence↗
Development of a microtitre ELISA to quantify development of Cryptosporidium parvum in vitro.
An in situ enzyme-linked immunosorbent assay (ELISA) was developed to evaluate growth of Cryptosporidium parvum in vitro. Ninety-six-well tissue culture microtitre plates were each seeded with 4.0 x 10(4) human ileocecal adenocarcinoma (HCT-8) cells, then infected with CsCl-purified oocysts 24 h later. The growth medium consisted of RPMI 1640 supplemented with 10% fetal bovine serum, 15 mM HEPES (N-2-hydroxyethylpiperazine N'-2-ethanesulfonic acid), 50 mM glucose, 1 microgram ml-1 folic acid, 4 micrograms ml-1 4-aminobenzoic acid, 2 micrograms ml-1 pantothenic acid and 35 micrograms ml-1 ascorbic acid. Incubation conditions were at 37 degrees C in a 5% CO2/95% humidified air incubator. Oocysts were allowed to excyst in situ so that sporozoites could infect cells directly. Monolayers were then washed, new medium added, and infected cells re-incubated. Levels of infection were assessed 48 h later using a rat anti-C. parvum polyvalent antiserum directed against purified parasite membranes, followed by a goat anti-rat IgG conjugated to horseradish peroxidase and 3,3',5,5'-tetramethyl-benzidine as substrate. Using various parasite inoculating doses and incubation times, optimal results were obtained using a 90-min exposure of host cells to 2.5-3.0 x 10(4) oocysts/well. Evaluation of various concentrations of four anti-microbials (monensin, lasalocid, paromomycin and sulfadimethoxine) in the system resulted in the acquisition of precise dose-response curves for each compound.
Animals↗
Pickles, pectin, and penicillin.
My professional life has been devoted to the study of microbial products and their biosynthesis, regulation, and overproduction. These have included primary metabolites (glutamic acid, tryptophan, inosinic acid, guanylic acid, vitamin B(12), riboflavin, pantothenic acid, ethanol, and lactic acid) and secondary metabolites (penicillin, cephalosporins, streptomycin, fosfomycin, gramicidin S, rapamycin, indolmycin, microcin B17, fumagillin, mycotoxins, Monascus pigments, and tetramethylpyrazine). Other areas included microbial nutrition, strain improvement, bioconversions of statins and beta-lactams, sporulation and germination, plasmid stability, gel microdroplets, and the production of double-stranded RNA, the polymer xanthan, and enzymes (polygalacturonase, protease, cellulase). Most of the studies were carried out with me by devoted and hardworking industrial scientists for 15 years at Merck & Co. and by similarly characterized students, postdoctorals, and visiting scientists during my 32 years at the Massachusetts Institute of Technology. I owe much of my success to my mentors from academia and industry. My recent research activities with undergraduate students at the Charles A. Dana Research Institute for Scientists Emeriti (R.I.S.E.) at Drew University have been very rewarding and are allowing me to continue my career.
Anti-Bacterial Agents↗
Fat-soluble and water-soluble vitamin contents of breast milk from Japanese women.
To determine the concentrations of fat-soluble and water-soluble vitamins in the maternal milk of Japanese women, we collected human milk samples from more than 4,000 mothers living throughout Japan between December 1998 and September 1999, and defined as group A the 691 samples among these that met the following conditions: breast milk of mothers who were under 40 y of age, who did not smoke habitually and/or use vitamin supplements, and whose babies showed no symptoms of atopy and had birth weights of 2.5 kg or more. We then analyzed the contents of vitamins individually. Large differences were observed among the contents of individual human milk samples. The mean contents of each component were as follows: vitamin A, 159.0 +/- 95.2 IU/100 mL; vitamin E, 0.325 +/- 0.165 alpha-TE mg/100mL; vitamin D3 (cholecalciferol), 8.0 +/- 10.7 ng/100mL; vitamin B1 (thiamin), 12.3 +/- 3.2 microg/100 mL; vitamin B2, 38.4 +/- 12.7 microg/100 mL; vitamin B6, 5.7 +/- 2.5 microg/100 mL; vitamin B12, 0.04 +/- 0.02 microg/100 mL; vitamin C, 5.1 +/- 1.9 mg/100 mL; biotin, 0.50 +/- 0.23 microg/100 mL; choline, 9.2 +/- 1.8 mg/100 mL; folic acid, 6.2 +/- 2.9 microg/100 mL; inositol, 12.6 +/- 3.6 mg/100 mL; niacin (nicotinamide), 32.9 +/- 20.4 microg/100 mL and pantothenic acid, 0.27 +/- 0.09 mg/100 mL. The concentrations of derivatives and/or related compounds of vitamin A (retinol, beta-carotene), vitamin E (alpha-, beta-, gamma-, and delta-tocopherol), and B2 (riboflavin, FMN, and FAD) were determined separately. The contents of each were found to vary greatly as the duration of lactation increased. The present results indicate that it is necessary to evaluate individual differences in human milk in order to perform valid research regarding infant formula.
Ascorbic Acid↗
Proliferation of peripheral blood mononuclear cells causes increased expression of the sodium-dependent multivitamin transporter gene and increased uptake of pantothenic acidopen star
Antigenic or mitogenic stimulation of peripheral blood mononuclear cells (PBMC) causes rapid cell proliferation. PBMC proliferation is associated with increased activities of pantothenic acid-dependent metabolic pathways, suggesting increased demand for pantothenic acid. We sought to determine whether PBMC respond to proliferation by increased cellular uptake of pantothenic acid and, if so, by what mechanism(s) the increased uptake is mediated. Uptake of pantothenic acid into PBMC was mediated by the sodium-dependent multivitamin transporter, SMVT, as judged by sodium dependency of uptake, substrate affinity and specificity, and RT-PCR of PBMC RNA. Proliferating PBMC accumulated two times more [3H]pantothenic acid than quiescent PBMC. Rates of [3H]pantothenic acid uptake paralleled rates of PBMC proliferation, as judged by uptake of [3H]thymidine. The increased uptake of [3H]pantothenic acid into proliferating PBMC was mediated by increased expression of SMVT (as judged by RT-PCR using total RNA from PBMC), leading to an increased number of transporters on the cell surface (as judged by maximal transport rates for pantothenic acid). We conclude that proliferating PBMC increase expression of the gene encoding SMVT to increase uptake of pantothenic acid.
Journal Article↗
[Metabolic acidosis and hypoglycemia during calcium hopantenate administration--report on 5 patients].
Calcium hopantenate (HOPA) has been widely used as an activator of cerebral metabolism in Japan. However, several cases of acute encephalopathy during HOPA administration were recently reported, which were characterized by marked metabolic acidosis and hypoglycemia. The encephalopathy in these patients was named Reye-like syndrome because of the similarity to Reye's syndrome in children. The purposes of this presentation are to report on 5 patients with acute encephalopathy developing during HOPA administration, to summarize their symptoms and clinical courses, and to discuss the pathogenesis of metabolic acidosis and hypoglycemia. Initial characteristics of the clinical course in all patients were loss of appetite, nausea and vomiting, followed by unconsciousness. Laboratory examinations revealed marked metabolic acidosis, severe hypoglycemia, hyperlactacidemia, leukocytosis, ketonuria, and increased Ht and BUN. A few days after development of the initial symptoms, mild renal and liver dysfunction, and elevation of serum amylase were observed in all patients. Hyperlactacidemia was present in 4 in the initial period. Blood concentration of HOPA was 2.131 micrograms/ml in patient 1 (8-10 hours after final administration), and 10.7 micrograms/ml in patient 5 (24 hours after final administration). These values are extremely high, because usually HOPA concentration is almost negligible 7 hours after the drug is taken. As the pathogenesis of acute encephalopathy due to HOPA administration, the failure of fatty acid beta-oxidation has been proposed by some investigators. However, the serum concentrations of CoA, pantothenic acid and carnitine during the initial stage were not reduced in our patients. Furthermore, it is very difficult to explain the severe hypoglycemia in terms of the beta-oxidation theory.(ABSTRACT TRUNCATED AT 250 WORDS)
Acidosis, Lactic↗
Synergistic growth promoting action of L-cysteine and nitrogen upon Hymenolepis diminuta cysticercoids in vitro.
Development in vitro of cysticercoids of the cestode Hymenolepis diminuta in the presence of L-cysteine proceeded twice as rapidly under 100% nitrogen as it did with air as the gas phase. No growth was obtained with the following: D-cysteine, L-cysteine methyl ester, S-aminoethyl cysteine, L-cystine, glutathione (reduced), L-methionine, D-pantothenic acid, taurine, or thioglycolic acid; limited growth only was obtained with ascorbic acid and dithiothreitol. Homocysteine or coenzyme A was as effective as L-cysteine in stimulating the complete development of oncospheres to cysticercoids. Experiments with 14C-L-cysteine indicated that L-cysteine was perhaps incorporated into the organisms.
Animals↗
A pantothenate auxotroph of Mycobacterium tuberculosis is highly attenuated and protects mice against tuberculosis.
With the advent of HIV and the widespread emergence of drug-resistant strains of Mycobacterium tuberculosis, newer control strategies in the form of a better vaccine could decrease the global incidence of tuberculosis. A desirable trait in an effective live attenuated vaccine strain is an ability to persist within the host in a limited fashion in order to produce important protective antigens in vivo. Attenuated M. tuberculosis vaccine candidates have been constructed by deleting genes required for growth in mice. These candidate vaccines did not elicit adequate protective immunity in animal models, due to their inability to persist sufficiently long within the host tissues. Here we report that an auxotrophic mutant of M. tuberculosis defective in the de novo biosynthesis of pantothenic acid (vitamin B5) is highly attenuated in immunocompromised SCID mice and in immunocompetent BALB/c mice. SCID mice infected with the pantothenate auxotroph survived significantly longer (250 days) than mice infected with either bacille Calmette-Guerin (BCG) vaccine or virulent M. tuberculosis (77 and 35 days, respectively). Subcutaneous immunization with this auxotroph conferred protection in C57BL/6J mice against an aerosol challenge with virulent M. tuberculosis, which was comparable with that afforded by BCG vaccination. Our findings highlight the importance of de novo pantothenate biosynthesis in limiting the intracellular survival and pathogenesis of M. tuberculosis without reducing its immunogenicity in vaccinated mice.
Animals↗
Mitochondrial, but not peroxisomal, beta-oxidation of fatty acids is conserved in coenzyme A-deficient rat liver.
Hepatic coenzyme A (CoA) plays an important role in cellular lipid metabolism. Because mitochondria and peroxisomes represent the two major subcellular sites of lipid metabolism, the present study was designed to investigate the specific impact of hepatic CoA deficiency on peroxisomal as well as mitochondrial beta-oxidation of fatty acids. CoA deficiency (47% decrease in free CoA and 23% decrease in total CoA) was produced by maintaining weanling male Sprague-Dawley rats on a semipurified diet deficient in pantothenic acid (the precursor of CoA) for 5 weeks. Hepatic mitochondrial fatty acid oxidation of short-chain and long-chain fatty acids were not significantly different between control and CoA-deficient rats. Conversely, peroxisomal beta-oxidation was significantly diminished (38% inhibition) in livers of CoA-deficient rats compared to control animals. Peroxisomal beta-oxidation was restored to normal levels when hepatic CoA was replenished. It is postulated that since the role of hepatic mitochondrial beta-oxidation is energy production while peroxisomal beta-oxidation acts mainly as a detoxification system, the mitochondrial pathway of beta-oxidation is spared at the expense of the peroxisomal pathway when liver CoA plummets. The present study may offer an animal model to investigate mechanisms involved in peroxisomal diseases.
Animals↗