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Results for “PANTOTHENIC ACID”

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At least 253 records · Page 14Linked to original sources
PubMed1996

Pantothenic acid and coenzyme A in experimental cisplatin-induced ototoxia.

We have observed that pantothenic acid (PA) prevents deafness induced by cisplatin (CP) in the guinea pig if both drugs are administered jointly. When deafness was previously produced, recovery was sometimes obtained after the administration of PA; so, we studied the effects of PA on cisplatian-induced ototoxia in guinea pigs, both as a prophylactic agent in healthy animals, and as a therapeutic agent in animals previously made deaf by the drug. To elucidate why PA protects the ear from the toxic effects of CP, we used coenzyme A (CoA) instead of PA-since PA is a component of CoA-to test the hypothesis that the action of PA is due to CoA. The results were practically the same in both experiences, the compound action potential of the auditory nerve (CAP) was tested and cochleas were examined by scanning electron microscopy (SEM). Our results suggest that the protective effect of PA takes place through CoA. Both substances had the same effect on CP ototoxicity, but CoA appears to be much more active, since the dose tested here was much lower than that of PA.

Animals↗
PubMedDate not supplied

[Metabolism of pantothenic acid and its derivatives in animals deficient in this enzyme].

Distribution of [14C]labelled metabolites of pantothenic acid (PAA) has been studied in tissues of normal and PAA-deficient rats-weaners 6 h after single injection of the calcium pantothenate (PAA-Ca), calcium 4'-phosphopantothenate (PAA-Ca) or pantethine (PT) preparations. Essential differences in the intertissue distribution of vitamin derivatives to be injected are revealed against a background of a higher vitamin-retaining ability of the PAA-deficient tissues. A degree of radionuclides' biotransformation into CoA permits them to be arranged in the series: PPA-Ca greater than PAA-Ca greater than PT. In PAA-deficient animals which were injected labelled PPA-Ca up to 41% of the liver radioactivity is concentrated in the CoA fraction and the quantity of label in the composition of PAA-protein cytosolium complexes increases considerably. It is supposed that there is a special PAA-depositing system which provides the intracellular CoA biosynthesis.

Animals↗
PubMed1981

Effect of exposure to cold on pantothenic acid metabolism in rat liver.

Exposure to a cold environment increased the incorporation of labeled pantothenic acid (PaA) into the liver and total PaA content. These increases were mainly due to an increase of free coenzyme A (CoA). The specific activity of the free CoA fraction was particularly high. These results suggest that exposure to a cold environment accelerates the rate of synthesis of CoA from PaA in the liver.

Animals↗
PubMed1984

[Antitoxic properties of pantothenic acid derivatives, precursors of coenzyme A biosynthesis, with regard to kanamycin].

The effect of calcium pantothenate (CPN)B 4'-phospho-CPN (PCP), pantetheine (PT) and calcium S-sulfopantetheine (SPN) on acute toxicity of kanamycin sulfate was studied on albino mice. The above derivatives of pantothenic acid except PT lowered the antibiotic toxicity. The coefficient of the antitoxic effect (LD50/ED50) of SPN and PCP was 1.3-1.4 times higher than that of CPN. The combined use of kanamycin (1/5 of the LD50) with CPN, PCP or PT (30 mg/kg bw was equivalent to CPN) for 15 days prevented the increase in the total content of CoA and in the content of the fraction of free CoA and the precursors of its biosynthesis participating in the reaction of N-acetylation in the liver and brain. The contents of these substances were within the normal during the whole experiment. A certain increase in the activity of pantothenate kinase in the liver cytosol due to the use of kanamycin was eliminated by the simultaneous use of PCP and PT. The vitamin-containing compounds PCP and SPN were recommended for the clinical trials as agents preventing complications of kanamycin therapy.

Animals↗
PubMed1988

Effects of ethanol and pantothenic acid on brain acetylcholine synthesis.

1. Measurements of brain acetylcholine (ACh) synthesis from precursor [14C]-pyruvate, pantothenic acid (PA) concentration in the brain, and blood ethanol (EtOH) concentration were made in rats treated with either ethanol (5-6 g kg-1 body wt daily) alone or ethanol with PA supplementation (100-200 mg kg-1 body wt daily). EtOH with or without PA was administered orally by either Lieber-Decarli liquid diet for 4 weeks and 4 months or by oral intubation for 1 and 4 days. Matched controls were given either ethanol-free liquid diet or saline. 2. ACh synthesis in the brain of rats treated with ethanol alone for 4 months was significantly (P less than 0.01) inhibited. PA concentration of the brain was diminished to 7.0% of the control value. 3. PA concentration in the brain of rats treated with ethanol plus PA for 4 months was three times that of rats treated with ethanol alone. ACh synthesis in rats with ethanol and PA supplementation was also significantly (P less than 0.01) higher. 4. There was no difference in blood EtOH concentration between rats treated with ethanol with or without PA supplement. 5. The EtOH effect on ACh synthesis and PA concentration in the brain was observed in the chronic treatments but not in the acute treatments. 6. Data suggest that chronic ethanol exposure may decrease ACh synthesis by depleting PA, a precursor for the synthesis of acetyl CoA. Acetyl CoA is an essential substrate for ACh synthesis.

Acetylcholine↗
PubMed1995

Pantothenic acid uptake and metabolism by red blood cells of rats.

Red blood cells (RBC) of rats and humans contain pantothenic acid (PA) derivatives, generally referred to as bound PA, which were never characterized or quantitated. This study was undertaken to define those factors that determine the rates of uptake and efflux of PA, and possibly PA derivatives, in RBC. Uptake of PA by RBC was studied by incubating RBC with different concentrations of PA (0.34-34.0 mumol/L), each containing [14C]PA (0.34 mumol/L) at 37 degrees C for 3-360 min. The effects of Na+, energy and pH on the uptake of PA in RBC were determined in experiments varying media concentrations of Na+ (0-152 mmol/L), glucose (0 and 10 mmol/L) or pH (7.2-7.6). The release of PA from RBC was studied by incubating RBC containing [14C]PA (0.10-10.4 nmol/10(7) RBC, final concentration) in fresh media at 37 degrees C for 10-240 min. Uptake and efflux of PA were found to be nonsaturable; uptake was not affected by Na+, energy or pH. Quantitative and qualitative determination of PA derivatives was by enzymatic hydrolysis of lysed RBC, followed by analysis of PA by RIA and paper chromatography. The RBC were found to contain PA, 4'-phosphopantothenic acid and pantetheine. We conclude that PA diffuses passively into and out of RBC and that RBC contain only PA, 4'-phosphopantothenic acid, pantetheine and no CoA.

Animals↗
PubMed2003

Long-term treatment of Barth syndrome with pantothenic acid: a retrospective study.

We report on three patients (two are brothers) with confirmed Barth syndrome treated with pantothenic acid. This treatment is still controversial and only one study has reported positive results to date. In our patients, long-term treatment has failed to reduce the number of infectious episodes and prevent dilated cardiomyopathy. Our cases show that this treatment is not as effective in Barth syndrome as was previously claimed.

Acyltransferases↗
PubMed1978

Effect of prenatal and neonatal pantothenic acid deficiency on rat intestinal phosphatases.

Alkaline phosphatase activity was increased in the distal part of the small intestine of pantothenic acid deficient neonatal rats, while acid phosphatase activity was slightly increased and protein concentration was decreased throughout the small intestine. The growth and maturation of the distal part of the small intestine were retarded more severely than in the proximal part.

Acid Phosphatase↗