COMMITTEE ON NUTRITION

PEDIATRICS ◽  
1966 ◽  
Vol 38 (6) ◽  
pp. 1068-1076
Author(s):  

Because of the limited information available it is not possible to derive precise figures for daily requirements of vitamin B6 in infants and children at this time. Data currently available suggest that the daily need in childhood is 0.5 to 1.5 mg and in adolescence is 1.5 to 2 mg. The requirement in infancy is clearly related to protein intake and is 20µg/gm of dietary protein. Requirements of a few individuals will undoubtedly be higher than the estimates for the normal population. Some of these patients will manifest frank biochemical and clinical signs of deficiency which will usually be promptly reversed by administration of small additional amounts of pyridoxine. Another group of patients will require large amounts of the vitamin to balance the heritable alteration in binding properties of a specific apoenzyme requiring pyridoxal phosphate for normal activity. It would appear that most infants, children and adults will have little difficulty in achieving an adequate intake of vitamin B6 if they receive what is considered to be in other respects an adequate diet.

2021 ◽  
Vol 22 (7) ◽  
pp. 3634
Author(s):  
Beata Szefler ◽  
Przemysław Czeleń ◽  
Przemysław Krawczyk

Platinum compounds have found wide application in the treatment of various types of cancer and carboplatin is one of the main platinum-based drugs used as antitumor agents. The anticancer activity of carboplatin arises from interacting with DNA and inducing programmed cell death. However, such interactions may occur with other chemical compounds, such as vitamins containing aromatic rings with lone-pair orbitals, which reduces the anti-cancer effect of carboplatin. The most important aspect of the conducted research was related to the evaluation of carboplatin affinity to vitamins from the B group and the potential impact of such interactions on the reduction of therapeutic capabilities of carboplatin in anticancer therapy. Realized computations, including estimation of Gibbs Free Energies, allowed for the identification of the most reactive molecule, namely vitamin B6 (pyridoxal phosphate). In this case, the computational estimations indicating carboplatin reactivity were confirmed by spectrophotometric measurements.


1959 ◽  
Vol 37 (3) ◽  
pp. 485-491 ◽  
Author(s):  
Edith G. McGeer ◽  
Bluma Tischler

Vitamin B6 was given to 10 phenylketonuric patients in doses up to 150 mg/day for a period of 9 weeks. Their clinical signs, behavior, intelligence, E.E.G.('s), serum phenylalanine levels, urinary phenylpyruvic acid and phenol levels, and excretions of ethyl-acetate-soluble aromatic derivatives were followed serially. No changes of significance to phenylketonuria were found, although chromatographic evidence indicated some changes in excretion of a few aromatic derivatives, notably Nα-acetyltryptophan.


Genes ◽  
2018 ◽  
Vol 10 (1) ◽  
pp. 8 ◽  
Author(s):  
Loes Loohuis ◽  
Monique Albersen ◽  
Simone de Jong ◽  
Timothy Wu ◽  
Jurjen Luykx ◽  
...  

The active form of vitamin B6, pyridoxal phosphate (PLP), is essential for human metabolism. The brain is dependent on vitamin B6 for its neurotransmitter balance. To obtain insight into the genetic determinants of vitamin B6 homeostasis, we conducted a genome-wide association study (GWAS) of the B6 vitamers pyridoxal (PL), PLP and the degradation product of vitamin B6, pyridoxic acid (PA). We collected a unique sample set of cerebrospinal fluid (CSF) and plasma from the same healthy human subjects of Dutch ancestry (n = 493) and included concentrations and ratios in and between these body fluids in our analysis. Based on a multivariate joint analysis of all B6 vitamers and their ratios, we identified a genome-wide significant association at a locus on chromosome 1 containing the ALPL (alkaline phosphatase) gene (minimal p = 7.89 × 10−10, rs1106357, minor allele frequency (MAF) = 0.46), previously associated with vitamin B6 levels in blood. Subjects homozygous for the minor allele showed a 1.4-times-higher ratio between PLP and PL in plasma, and even a 1.6-times-higher ratio between PLP and PL in CSF than subjects homozygous for the major allele. In addition, we observed a suggestive association with the CSF:plasma ratio of PLP on chromosome 15 (minimal p = 7.93 × 10−7, and MAF = 0.06 for rs28789220). Even though this finding is not reaching genome-wide significance, it highlights the potential of our experimental setup for studying transport and metabolism across the blood–CSF barrier. This GWAS of B6 vitamers identifies alkaline phosphatase as a key regulator in human vitamin B6 metabolism in CSF as well as plasma. Furthermore, our results demonstrate the potential of genetic studies of metabolites in plasma and CSF to elucidate biological aspects underlying metabolite generation, transport and degradation.


2020 ◽  
Vol 39 (9) ◽  
pp. 2824-2831 ◽  
Author(s):  
Dinesh Talwar ◽  
Anthony Catchpole ◽  
John M. Wadsworth ◽  
Barry J. Toole ◽  
Donald C. McMillan

2020 ◽  
Vol 7 (4) ◽  
pp. 192
Author(s):  
Maria Chiara Marchesi ◽  
Giulia Moretti ◽  
Giovanni Angeli ◽  
Francesco Birettoni ◽  
Francesco Porciello ◽  
...  

A 13-year-old male mixed-breed dog was examined because of hematuria and pyrexia. Ultrasonographic examination of the genitourinary tract showed the presence of a migrating grass awn in the right prostatic lobe. Laparotomy allowed, under ultrasonographic guidance, to remove entirely the migrating grass awn from the prostatic parenchyma. The recovery was uneventful and four months after the surgery the owner reported that the dog showed the complete resolution of the clinical signs and full return to normal activity. To our knowledge, this case report describes for the first time the clinical presentation, imaging findings, management and outcome for a dog with prostatic localization of a migrating grass awn.


1979 ◽  
Vol 13 (10) ◽  
pp. 1097-1100
Author(s):  
M. A. Kovler ◽  
Zh. P. Alekseeva ◽  
T. N. Smirnova ◽  
M. L. Lobanova ◽  
L. A. Shevnyuk ◽  
...  

2019 ◽  
Vol 4 (2) ◽  

Delayed Puberty (DP), especially in boys, is a common presentation in paediatrics. By definition DP is defined as the presentation of clinical signs of puberty 2-2.5SD later than in the normal population. With the recent advances in understanding of the neuroendocrine, genetic and environmental factors controlling pubertal development it has become easier to understand the pathophysiology of DP. The discovery of kisspeptin signaling through its receptor identified neuroendocrine mechanisms controlling the gonadotropin releasing hormone (GnRH) pulse generator at the onset of puberty. Genetic mechanisms from single gene mutations to single nucleotide polymorphisms associated with DP are being identified. Environmental factors, including nutritional factors, besides endocrine disruptors, have been associated with the secular trends and abnormal timing of puberty. Inspite of these advances, the main question remains how to differentiate DP associated with underlying pathology of hypogonadism from constitutional delay in growth and puberty (CDP) that remains challenging as biochemical tests do not always discriminate the 2.The diagnostic accuracies of newer investigations which include the 36-hour luteininzing hormone releasing hormone(LHRH) tests, GnRH agonist tests, antimullerian hormone and inhibin B, need further evaluation. Sex hormone replacement remains the main therapy that is available for DP, whose choice is based on clinical practice and the availability of the various sex steroid preparations. Spontaneous reversal of hypogonadism has been reported in boys having idiopathic hypogonadotropic hypogonadism following sex steroid treatment, which highlights the importance of reassessment at the end of pubertal induction .Novel therapies having a more physiological bases like gonadotropins or kisspeptin agonists are getting investigated for the management of hypogonadotropic hypogonadism. A careful assessment and knowledge of the normal physiology remains the mainstay of managing patients with DP.


2021 ◽  
Vol 11 ◽  
Author(s):  
Akram A. Da’dara ◽  
Manal Elzoheiry ◽  
Samar N. El-Beshbishi ◽  
Patrick J. Skelly

Schistosomes are parasitic platyhelminths that currently infect >200 million people globally. The adult worms can live within the vasculature of their hosts for many years where they acquire all nutrients necessary for their survival and growth. In this work we focus on how Schistosoma mansoni parasites acquire and metabolize vitamin B6, whose active form is pyridoxal phosphate (PLP). We show here that live intravascular stage parasites (schistosomula and adult males and females) can cleave exogenous PLP to liberate pyridoxal. Of the three characterized nucleotide-metabolizing ectoenzymes expressed at the schistosome surface (SmAP, SmNPP5, and SmATPDase1), only SmAP hydrolyzes PLP. Heat-inactivated recombinant SmAP can no longer cleave PLP. Further, parasites whose SmAP gene has been suppressed by RNAi are significantly impaired in their ability to cleave PLP compared to controls. When schistosomes are incubated in murine plasma, they alter its metabolomic profile—the levels of both pyridoxal and phosphate increase over time, a finding consistent with the action of host-exposed SmAP acting on PLP. We hypothesize that SmAP-mediated dephosphorylation of PLP generates a pool of pyridoxal around the worms that can be conveniently taken in by the parasites to participate in essential, vitamin B6-driven metabolism. In addition, since host PLP‐dependent enzymes play active roles in inflammatory processes, parasite-mediated cleavage of this metabolite may serve to limit parasite-damaging inflammation. In this work we also identified schistosome homologs of enzymes that are involved in intracellular vitamin B6 metabolism. These are pyridoxal kinase (SmPK) as well as pyridoxal phosphate phosphatase (SmPLP-Ph) and pyridox(am)ine 5’-phosphate oxidase (SmPNPO) and cDNAs encoding these three enzymes were cloned and sequenced. The three genes encoding these enzymes all display high relative expression in schistosomula and adult worms suggestive of robust vitamin B6 metabolism in the intravascular life stages.


PEDIATRICS ◽  
1956 ◽  
Vol 17 (1) ◽  
pp. 92-92

The experiments reported in this paper are directed at a possible antimetabolite relationship between isoniazid and pyridoxine. The effects of vitamin B6 deficiency alone, vitamin B6 deficiency plus isoniazid and vitamin B6 deficiency plus desoxypyridoxine administration were observed. The symptoms of pyridoxine deficiency were aggravated by both isoniazid and desoxypyridoxine but the two compounds produced different effects on certain of the manifestations of vitamin B6 deficiency. The paper is of considerable theoretical interest in demonstrating that antimetabolites may differ in the intensity that they affect the functions of the compound with which they are in conflict. The results further emphasize the possible clinical significance of vitamin B6 deficiency occurring in patients undergoing isoniazid therapy for tuberculosis. The toxic effects of isoniazid which simulate vitamin B6 deficiency may be prevented by assuring an adequate intake of vitamin B6 during therapy. Amounts of vitamin B6 which meet the daily requirements do not appear to affect the antituberculosis activity of isoniazid.


Sign in / Sign up

Export Citation Format

Share Document