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PubMed2004

Micronutrient intake during pregnancy in relation to birth size.

BACKGROUND: There exists very little information on possible effects on birth size of micronutrient intakes at levels that are usually encountered among pregnant women in developed countries. AIM OF THE STUDY: To examine the relation of the intake of 20 micronutrients with birth weight, placental weight, birth length and head circumference of the offspring. METHODS: In a cohort of 222 Caucasian women with singleton pregnancies in Boston, USA, diet during pregnancy was ascertained at the 27th gestational week through a validated semi-quantitative food frequency questionnaire, covering also intake of dietary supplements. Micronutrient intakes were correlated with birth size parameters after adjustment for confounding variables, including total energy intake. RESULTS: Pantothenic acid, sodium and vitamin E were positively associated with all four birth size parameters. For pantothenic acid the association was statistically significant with respect to birth length, whereas for sodium with respect to head circumference and for vitamin E with respect to birth weight. In contrast, zinc was inversely associated with all four birth size parameters and the association was statistically significant with respect to head circumference. CONCLUSIONS: In a moderately sized prospective study, we found evidence that pregnancy intake of pantothenic acid, vitamin E and sodium may be positively related with at least one of the studied birth size parameters, whereas an inverse association was found with respect to zinc intake. For the remaining 16 micronutrients, our findings indicate that they are not associated with birth size, at least within the range of intake encountered in this investigation. The results of this exploratory analysis need to be confirmed before pathophysiologic interpretations and generalizations are attempted.

Adolescent↗
PubMedDate not supplied

[Cysteine effects on yeast growth].

The effect of cysteine on yeasts with different requirements for exogenous pantothenic acid was studied during their cultivation in the synthetic nutrient medium. Cysteine added at a concentration of 4X10(-4) M and 6X10(-4) M inhibited the growth of Saccharomyces cerevisiae of the Krasnodarsk race and Candida utilis BKM y-74 to a great extent and that of Saccharomycodes ludwigii BKM y-1176 to a lesser extent. The inhibitory effect of cystein was reversed by pantothenic acid, beta-alanine, aspartate and aspartic acid. It is assumed that cysteine inhibits metabolic utilization of pantothenic acid.

Alanine↗
PubMed2002

The antibiotic activity of N-pentylpantothenamide results from its conversion to ethyldethia-coenzyme a, a coenzyme a antimetabolite.

Pantothenic acid (vitamin B(5)) is the natural precursor of coenzyme A (CoA), an essential cofactor in all organisms. The pantothenic acid antimetabolite N-pentylpantothenamide inhibits the growth of Escherichia coli with a minimum inhibitory concentration of 2 microm. In this study, we examine the mechanism of this inhibition. Using the last five enzymes of the CoA biosynthetic pathway in E. coli we demonstrate that N-pentylpantothenamide does not inhibit the CoA biosynthetic enzymes but instead acts as an alternative substrate, forming the CoA analog ethyldethia-CoA. We show that N-pentylpantothenamide is converted to ethyldethia-CoA 10.5 times faster than CoA is biosynthesized from pantothenic acid, demonstrating that ethyldethia-CoA biosynthesis can effectively compete with CoA biosynthesis in the cell. We conclude that the mechanism of toxicity of N-pentylpantothenamide is most likely due to its biosynthetic conversion to the CoA analog ethyldethia-CoA, which may act as an inhibitor of CoA- and acetyl-CoA-utilizing enzymes.

Anti-Bacterial Agents↗
PubMed1983

A high yield method for the preparative synthesis of coenzyme A by combination of chemical and enzymic reactions.

Dried cells of Brevibacterium ammoniagenes are a good enzyme source for the preparative synthesis of CoA from pantothenic acid, L-cysteine and ATP. A problem with this synthesis is that the CoA synthesis is repressed by negative feedback inhibition by CoA to pantothenate kinase, the first step enzyme for the biosynthesis of CoA, which catalyses phosphorylation of pantothenic acid or pantetheine. As the inhibition operates only at this step, a further increased yield is possible if the enzymic phosphorylation step is replaced with chemical synthesis. Yields from phosphorylated substrates are more than 10-times higher than those from pantothenic acid or pantetheine (33 g/l from phosphopantothenic acid with a molar yield of 86%; 115 g/l from phosphopantetheine with a molar yield of 100%).

Brevibacterium↗
PubMed2001

The biosynthesis of coenzyme A in bacteria.

Coenzyme A (I) and enzyme-bound phosphopantetheine (II) function as acyl carriers and as carbonyl activating groups for Claisen reactions as well as for amide-, ester-, and thioester-forming reactions in the cell. In so doing, these cofactors play a key role in the biosynthesis and breakdown of fatty acids and in the biosynthesis of polyketides and nonribosomal peptides. Coenzyme A is biosynthesized in bacteria in nine steps. The biosynthesis begins with the decarboxylation of aspartate to give beta-alanine. Pantoic acid is formed by the hydroxymethylation of alpha-ketoisovalerate followed by reduction. These intermediates are then condensed to give pantothenic acid. Phosphorylation of pantothenic acid followed by condensation with cysteine and decarboxylation gives 4'-phosphopantetheine. Adenylation and phosphorylation of 4'-phosphopantetheine completes the biosynthesis of coenzyme A. This review will focus on the mechanistic enzymology of coenzyme A biosynthesis in bacteria.

Coenzyme A↗