Vitamin A
(Synonyms: 维生素A) 目录号 : GC37913
An intermediate in retinol metabolism
Cas No.:11103-57-4
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Vitamin A, also known as all-trans retinol, is an intermediate in retinol metabolism in animals. It is metabolized to retinoic acid , a ligand for both the retinoic acid receptor (RAR) and the retinoid X receptor (RXR). RAR and RXR heterodimerize and act as ligand-dependent transcriptional regulators, with roles in development, reproduction, immunity, organogenesis, and cancer.1,2,3
1.Duong, V., and Rochette-Egly, C.The molecular physiology of nuclear retinoic acid receptors. From health to diseaseBiochim. Biophys. Acta1812(8)1023-1031(2011) 2.Rochette-Egly, C., and Germain, P.Dynamic and combinatorial control of gene expression by nuclear retinoic acid receptors (RARs)Nucl. Recept. Signal7e005(2009) 3.Dollé, P.Developmental expression of retinoic acid receptors (RARs)Nucl. Recept. Signal71-13(2009)
| Cas No. | 11103-57-4 | SDF | |
| 别名 | 维生素A | ||
| Canonical SMILES | [Vitamin A] | ||
| 分子式 | 分子量 | ||
| 溶解度 | Chloroform: 10 mg/ml,DMF: 30 mg/ml,DMSO: 30 mg/ml,Ethanol: 10 mg/ml | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
The importance of Vitamin A in nutrition
Curr Pharm Des 2000 Feb;6(3):311-25.PMID:10637381DOI:10.2174/1381612003401190.
Preformed Vitamin A (all-trans-retinol and its esters) and provitamin A (beta-carotene) are essential dietary nutrients that provide a source of retinol. Both retinyl esters and beta-carotene are metabolized to retinol. The retinol-binding proteins on binding retinol provide a means for solubilizing retinol for delivery to target tissues and for regulating retinol plasma concentrations. Oxidation of retinol provides retinal, which is essential for vision, and retinoic acid, a transcription factor ligand that has important roles in regulating genes involved in cell morphogenesis, differentiation, and proliferation. The observations that Vitamin A can produce cell and tissue changes similar to those found during neoplastic transformation and that vitamin supplementation can reverse this process indicated a potential role for Vitamin A in cancer prevention. Thus far, correlative epidemiological studies on Vitamin A use and cancer prevention have produced mixed results, as this review indicates. Apparently, in populations deficient in Vitamin A (caused by an inadequate diet or tobacco use), supplementation programs appear to be effective in reducing cancer incidence. In groups already having sufficient dietary or supplemental Vitamin A, cancer prevention by added Vitamin A may not be particularly effective. The most likely reason for the low efficacy in the latter groups is that feedback mechanisms that increase retinol storage in the liver limit retinol plasma levels; whereas, supplementation at higher doses causes toxicity. In addition to serving as a metabolic source of retinol, beta-carotene, along with other dietary carotenoids, function as antioxidants that can prevent carcinogenesis by decreasing the levels of the free-radicals that cause DNA damage.
Vitamin A and the epigenome
Crit Rev Food Sci Nutr 2017 Jul 24;57(11):2404-2411.PMID:26565606DOI:10.1080/10408398.2015.1060940.
The epigenetic phenomena refer to heritable changes in gene expression other than those in the DNA sequence, such as DNA methylation and histone modifications. Major research progress in the last few years has provided further proof that environmental factors, including diet and nutrition, can influence physiologic and pathologic processes through epigenetic alterations, which in turn influence gene expression. This influence is termed nutritional epigenetics, and one prominent example is the regulation of gene transcription by Vitamin A through interaction to its nuclear receptor. Vitamin A is critical throughout life. Together with its derivatives, it regulates diverse processes including reproduction, embryogenesis, vision, growth, cellular differentiation and proliferation, maintenance of epithelial cellular integrity and immune function. Here we review the epigenetic role of Vitamin A in cancer, stem cells differentiation, proliferation, and immunity. The data presented here show that retinoic acid is a potent agent capable of inducing alterations in epigenetic modifications that produce various effects on the phenotype. Medical benefits of Vitamin A as an epigenetic modulator, especially with respect to its chronic use as nutritional supplement, should rely on our further understanding of its epigenetic effects during health and disease, as well as through different generations.
Illuminating the Role of Vitamin A in Skin Innate Immunity and the Skin Microbiome: A Narrative Review
Nutrients 2021 Jan 21;13(2):302.PMID:33494277DOI:10.3390/nu13020302.
Vitamin A is a fat-soluble vitamin that plays an important role in skin immunity. Deficiencies in Vitamin A have been linked to impaired immune response and increased susceptibility to skin infections and inflammatory skin disease. This narrative review summarizes recent primary evidence that elucidates the role of Vitamin A and its derivatives on innate immune regulators through mechanisms that promote skin immunity and sustain the skin microbiome.
Vitamin A in health care: Suppression of growth and induction of differentiation in cancer cells by Vitamin A and its derivatives and their mechanisms of action
Pharmacol Ther 2022 Feb;230:107942.PMID:34175370DOI:10.1016/j.pharmthera.2021.107942.
Vitamin A is an important micro-essential nutrient, whose primary dietary source is retinyl esters. In addition, β-carotene (pro-vitamin A) is a precursor of Vitamin A contained in green and yellow vegetables that is converted to retinol in the body after ingestion. Retinol is oxidized to produce visual retinal, which is further oxidized to retinoic acid (RA), which is used as a therapeutic agent for patients with promyelocytic leukemia. Thus, the effects of retinal and RA are well known. In this paper, we will introduce (1) Vitamin A circulation in the body, (2) the actions and mechanisms of retinal and RA, (3) retinoylation: another RA mechanism not depending on RA receptors, (4) the relationship between cancer and actions of retinol or β-carotene, whose roles in vivo are still unknown, and (5) anti-cancer actions of Vitamin A derivatives derived from fenretinide (4-HPR). We propose that Vitamin A nutritional management is effective in the prevention of cancer.
Biological evidence to define a Vitamin A deficiency cutoff using total liver Vitamin A reserves
Exp Biol Med (Maywood) 2021 May;246(9):1045-1053.PMID:33765844DOI:10.1177/1535370221992731.
Vitamin A is a fat-soluble vitamin involved in essential functions including growth, immunity, reproduction, and vision. The Vitamin A Dietary Reference Intakes (DRIs) for North Americans suggested that a minimally acceptable total liver Vitamin A reserve (TLR) is 0.07 µmol/g, which is not explicitly expressed as a Vitamin A deficiency cutoff. The Biomarkers of Nutrition for Development panel set the TLR cutoff for Vitamin A deficiency at 0.1 µmol/g based on changes in biological response of several physiological parameters at or above this cutoff. The criteria used to formulate the DRIs include clinical ophthalmic signs of Vitamin A deficiency, circulating plasma retinol concentrations, excretion of Vitamin A metabolites in the bile, and long-term storage of Vitamin A as protection against Vitamin A deficiency during times of low dietary intake. This review examines the biological responses that occur as TLRs are depleted. In consideration of all of the DRI criteria, the review concludes that induced biliary excretion and long-term Vitamin A storage do not occur until TLRs are >0.10 µmol/g. If long-term storage is to continue to be part of the DRI criteria, Vitamin A deficiency should be set at a minimum cutoff of 0.10 µmol/g and should be set higher during times of enhanced requirements where TLRs can be rapidly depleted, such as during lactation or in areas with high infection burden. In population-based surveys, cutoffs are important when using biomarkers of micronutrient status to define the prevalence of deficiency and sufficiency to inform public health interventions. Considering the increasing use of quantitative biomarkers of Vitamin A status that indirectly assess TLRs, i.e. the modified-relative-dose response and retinol-isotope dilution tests, setting a TLR as a Vitamin A deficiency cutoff is important for users of these techniques to estimate Vitamin A deficiency prevalence. Future researchers and policymakers may suggest that DRIs should be set with regard to optimal health and not merely to prevent a micronutrient deficiency.