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Vitamin A

$155

  • Brand : BIOFRON

  • Catalogue Number : BF-V1001

  • Specification : 98%

  • CAS number : 68-26-8

  • Formula : C20H30O

  • Molecular Weight : 286.45

  • PUBCHEM ID : 445354

  • Volume : 20mg

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Catalogue Number

BF-V1001

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

286.45

Appearance

Yellow paste

Botanical Source

Structure Type

Terpenoids

Category

Standards;Natural Pytochemical;API

SMILES

CC1=C(C(CCC1)(C)C)C=CC(=CC=CC(=CCO)C)C

Synonyms

Alphalin/Lard-factor/Vitamin A1/(2E,4E,6E,8E)-3,7-dimethyl-9-(2,6,6-trimethylcyclohexen-1-yl)nona-2,4,6,8-tetraen-1-ol/3,7-Dimethyl-9-(2,6,6-trimethyl-1-cyclohexen-1-yl)-2,4,6,8-nonatetraen-1-ol/Vitamin A (USP)/trans-retinol/Vitamine A/Vitaminum A/Retinol/VI-a/Vitamin A/(2E,4E,6E,8E)-3,7-Dimethyl-9-(2,6,6-trimethyl-1-cyclohexen-1-yl)-2,4,6,8-nonatetraen-1-ol/TRANS-VITAMIN A ALCOHOL/all-trans-retinol/(2E,4E,6E,8E)-3,7-dimethyl-9-(2,6,6-trimethylcyclohex-1-en-1-yl)nona-2,4,6,8-tetraen-1-ol/(2E,4E,6E,8E)-3,7-Dimethyl-9-(2,6,6-trimethyl-1-cyclohexen-1-yl)-2,4,6,8-nonatetraen-1-ol/Vitamin A1 alcohol, all-trans-

IUPAC Name

(2E,4E,6E,8E)-3,7-dimethyl-9-(2,6,6-trimethylcyclohexen-1-yl)nona-2,4,6,8-tetraen-1-ol

Density

1.0±0.1 g/cm3

Solubility

Methanol; Chloroform

Flash Point

147.3±16.4 °C

Boiling Point

421.2±14.0 °C at 760 mmHg

Melting Point

61-63 °C(lit.)

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2936210000

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:68-26-8) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

31940621

Abstract

Vitamins are essential organic compounds that catalyze metabolic reactions. They also function as electron donors, antioxidants or transcription effectors. They can be extracted from food and supplements, or in some cases, synthesized by our body or gut microbiome. Severe vitamin deficiencies result in systemic complications, including the development of scurvy, rickets, pellagra, and beriberi. Some moderate and severe deficiencies also result in oral conditions. A lower intake of vitamin A has been associated with decreased oral epithelial development, impaired tooth formation, enamel hypoplasia and periodontitis. Vitamin D deficiency during tooth development may result in non-syndromic amelogenesis and dentinogenesis imperfecta, enamel and dentin hypoplasia, and dysplasia. Clinical studies have demonstrated an association between vitamin D’s endocrine effects and periodontitis. On the other hand, no significant association has been found between cariogenic activity and vitamin D deficiency. Vitamin C deficiency results in changes in the gingivae and bone, as well as xerostomia; while vitamin B deficiencies are associated with recurrent aphthous stomatitis, enamel hypomineralization, cheilosis, cheilitis, halitosis, gingivitis, glossitis, atrophy of the lingual papillae, stomatitis, rashes around the nose, dysphagia, and pallor. The effects of vitamins E and K on oral health are not as clear as those of other vitamins. However, vitamin K has a systemic effect (increasing the risk of haemorrhage), which may affect individuals undergoing oral surgery or suffering an oral injury. Health care professionals need to be aware of the effects of vitamins on oral health to provide the best available care for their patients.

© 2020 S. Karger AG, Basel.

Title

Chapter 6: Vitamins and Oral Health.

Author

Gutierrez Gossweiler A1, Martinez-Mier EA2.

Publish date

2020;

PMID

31931077

Abstract

Failure of all-trans-retinal (atRAL) clearance contributes to retina degeneration. However, whether autophagy can be activated by excess atRAL accumulation in retinal pigment epithelial (RPE) cells is not known. This study showed that atRAL provoked mitochondria-associated reactive oxygen species (ROS) production, activated the nuclear factor (erythroid-derived 2)-like 2 and apoptosis in a human RPE cell line, ARPE-19 cells. Moreover, we found that autophagic flux was functionally activated after atRAL treatment. The antioxidant N-acetylcysteine attenuated the expression of autophagy markers, suggesting that ROS triggered atRAL-activated autophagy. In addition, autophagic cell death was observed in atRAL-treated RPE cells, while inhibition of autophagy with 3-methyladenine or LC3, Beclin1, p62 silencing ameliorated atRAL-induced cytotoxicity. Suppression of autophagy quenched mitochondrial ROS and inhibited HO-1 and γ-GCSh expression, indicating that atRAL-activated autophagy enhances intracellular oxidative stress, thereby promoting RPE cell apoptosis. Furthermore, we found that inhibiting endoplasmic reticulum (ER) stress suppressed atRAL-induced mitochondrial ROS generation, subsequently attenuated autophagy and apoptosis in RPE cells. Taken together, these results suggest that atRAL-induced oxidative stress and ER stress modulate autophagy, which may contribute to RPE degeneration. There may be positive feedback regulatory mechanisms between atRAL-induced oxidative stress and autophagy or ER stress.

Copyright © 2020 Elsevier B.V. All rights reserved.

KEYWORDS

All-trans-retinal; Autophagic cell death; Autophagy; Endoplasmic reticulum stress; Oxidative stress; Retinal pigment epithelial cell

Title

All-trans-retinal induces autophagic cell death via oxidative stress and the endoplasmic reticulum stress pathway in human retinal pigment epithelial cells.

Author

Zhang L1, Zhou Y1, Xia Q1, Chen Y1, Li J2.

Publish date

2020 Apr 1

PMID

31865950

Abstract

In accordance with World Health Organization guidelines, South Africa (SA) introduced routine periodic high-dose vitamin A supplementation (VAS) in 2002. These guidelines were developed after research in the 1980s and 1990s showed the efficacy of VAS in reducing childhood mortality. However, two recent studies in low- to middle-income countries (2013 and 2014) have shown no effect of high-dose VAS on mortality. Additionally, there is no clear research evidence that 6-monthly doses of vitamin A result in a sustained shift in serum retinol levels or reduce subclinical vitamin A deficiency. These two points should encourage SA to re-examine the validity of these guidelines. A long-term view of what is in the best interests of the majority of the people is needed. The short-term intervention of administering vitamin A capsules not only fails to improve serum retinol levels but may create dependence on a ‘technical fix’ to address the fundamental problem of poor nutrition, which is ultimately underpinned by poverty. It may also cause harm. Although there are those, some with vested interests, who will argue for continuation of the routine high-dose VAS programmes, SA policymakers and scientists need to evaluate the facts and be prepared to rethink this policy. There is cause for optimism: SA’s health policymakers have previously taken bold stands on the basis of evidence. The examples of regulation of tobacco products and taxation of sugar-sweetened beverages, ending the free distribution of formula milk for HIV-positive mothers and legislating against the marketing of breastmilk substitutes provide precedents. Here is a time yet again for decision-makers to make bold choices in the interests of the people of SA. While the cleanest choice would be national discontinuation of the routine VAS programme, there may be other possibilities, such as first stopping the programme in Northern Cape Province (where there is clear evidence of hypervitaminosis A), followed by the other provinces in time.

Title

Is it time for South Africa to end the routine high-dose vitamin A supplementation programme?

Author

Coutsoudis A1, Sanders D, Dhansay MA, Van Stuijvenberg ME, Benn CS.

Publish date

2019 Nov 27


Description :

Retinol, also known as Vitamin A1, has pleiotropic functions including vison, immunity, hematopoiesis, reproduction, cell differentiation/growth, and development.