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Retinol (Vitamin A1) Sale

(Synonyms: 视黄醇) 目录号 : GC31345

An intermediate in retinol metabolism

Retinol (Vitamin A1) Chemical Structure

Cas No.:68-26-8

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10mM (in 1mL DMSO)
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100mg
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实验参考方法

Kinase experiment:

Activity of alcohol dehydrogenases (ADHs)/retinol dehydrogenases (RDHs) and retinal dehydrogenases (RALDHs) are assessed. Briefly, hepatic ADHs/RDHs and RALDHs activities are evaluated with Retinal formation in the presence of β-nicotinamide adenine dinucleotide (β-NAD+) and β-Nicotinamide adenine dinucleotide phosphate (β-NADP+), respectively. The incubation mixture consists of hepatic cytosol/microsomes (at the final concentration of 0.5 mg/mL), and a series concentrations of Retinol, 4.0 mM co-factor, 5 mM MgCl2, 91 μM butylated hydroxytoluene in a total volume of 500 μL. The reaction is initiated by the addition of Retinol pre-incubated for 5 min at 37°C. Following 15 min incubation, the reaction is quenched by extraction with equal volume of n-butanol/methanol, 95:5 (v:v) containing 0.005% butylated hydroxytoluene[1].

Animal experiment:

Wistar rats (male, aged 4 wk) are used in this study. Two groups of 6 rats are given free access to the following diets: the standard diet (control group) and the methionine-choline deficient diet (MCD) group. Each diet contains Retinol (1000 IU/100g). After 6 wk, the rats are sacrificed by exsanguination under isoflurane anesthesia after an overnight fast. Blood is collected in heparinized tubes, and plasma is separated for storage at -80°C. The liver, intestine, testes, and kidneys are removed, immediately frozen in liquid nitrogen, and stored at -80°C[2].

References:

[1]. Zhang M, et al. High-fat diet enhanced retinal dehydrogenase activity, but suppressed retinol dehydrogenase activity in liver of rats. J Pharmacol Sci. 2015 Apr;127(4):430-8.
[2]. Miyazaki H, et al. Retinol status and expression of retinol-related proteins in methionine-choline deficient rats. J Nutr Sci Vitaminol (Tokyo). 2014;60(2):78-85.

产品描述

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)

Chemical Properties

Cas No. 68-26-8 SDF
别名 视黄醇
Canonical SMILES CC(/C=C/C=C(/C=C/C1=C(CCCC(C)1C)C)C)=C\CO
分子式 C20H30O 分子量 286.45
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
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1 mM 3.491 mL 17.4551 mL 34.9101 mL
5 mM 0.6982 mL 3.491 mL 6.982 mL
10 mM 0.3491 mL 1.7455 mL 3.491 mL
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Research Update

The Role of Vitamin A in Wound Healing

Vitamin A is an essential micronutrient that comes in multiple forms, including retinols, retinals, and retinoic acids. Dietary vitamin A is absorbed as retinol from preformed retinoids or as pro-vitamin A carotenoids that are converted into retinol in the enterocyte. These are then delivered to the liver for storage via chylomicrons and later released into the circulation and to its biologically active tissues bound to retinol-binding protein. Vitamin A is a crucial component of many important and diverse biological functions, including reproduction, embryological development, cellular differentiation, growth, immunity, and vision. Vitamin A functions mostly through nuclear retinoic acid receptors, retinoid X receptors, and peroxisome proliferator-activated receptors. Retinoids regulate the growth and differentiation of many cell types within skin, and its deficiency leads to abnormal epithelial keratinization. In wounded tissue, vitamin A stimulates epidermal turnover, increases the rate of re-epithelialization, and restores epithelial structure. Retinoids have the unique ability to reverse the inhibitory effects of anti-inflammatory steroids on wound healing. In addition to its role in the inflammatory phase of wound healing, retinoic acid has been demonstrated to enhance production of extracellular matrix components such as collagen type I and fibronectin, increase proliferation of keratinocytes and fibroblasts, and decrease levels of degrading matrix metalloproteinases.

The importance of vitamin A in nutrition

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.

Efect of vitamin A suplementation: a systematic review

To evaluate the effect of vitamin A supplementation in postpartum infants and women on serum retinol levels and breast milk. The databases Medline, PubMed, Lilacs and SciELO were consulted. The descriptors used were vitamin A, dietary supplement, child, postpartum period, infant and nutrition programs policies. Search found 7432 articles. After elimination of duplicity and application of eligibility criteria, 8 studies remained. All evaluated the effect of vitamin A supplementation on immediate postpartum, five studies used retinyl palmitate supplementation, one with retinyl palmitate and two did not specify the form of supplementation. Six studies evaluated colostrum and two included supplementation of children. It was found that supplementation in the puerperium increases the concentrations of serum retinol and breast milk, however, this result was in the short term and was relevant when the previous concentrations of the mother were low. When maternal serum concentrations are adequate, the retinol content in milk does not change, with little relevance for children. Further studies should be performed to evaluate the effect of megadoses supplementation on serum concentrations of children.

Vitamin a metabolism, action, and role in skeletal homeostasis

Vitamin A (retinol) is ingested as either retinyl esters or carotenoids and metabolized to active compounds such as 11-cis-retinal, which is important for vision, and all-trans-retinoic acid, which is the primary mediator of biological actions of vitamin A. All-trans-retinoic acid binds to retinoic acid receptors (RARs), which heterodimerize with retinoid X receptors. RAR-retinoid X receptor heterodimers function as transcription factors, binding RAR-responsive elements in promoters of different genes. Numerous cellular functions, including bone cell functions, are mediated by vitamin A; however, it has long been recognized that increased levels of vitamin A can have deleterious effects on bone, resulting in increased skeletal fragility. Bone mass is dependent on the balance between bone resorption and bone formation. A decrease in bone mass may be caused by either an excess of resorption or decreased bone formation. Early studies indicated that the primary skeletal effect of vitamin A was to increase bone resorption, but later studies have shown that vitamin A can not only stimulate the formation of bone-resorbing osteoclasts but also inhibit their formation. Effects of vitamin A on bone formation have not been studied in as great a detail and are not as well characterized as effects on bone resorption. Several epidemiological studies have shown an association between vitamin A, decreased bone mass, and osteoporotic fractures, but the data are not conclusive because other studies have found no associations, and some studies have suggested that vitamin A primarily promotes skeletal health. In this presentation, we have summarized how vitamin A is absorbed and metabolized and how it functions intracellularly. Vitamin A deficiency and excess are introduced, and detailed descriptions of clinical and preclinical studies of the effects of vitamin A on the skeleton are presented.

Biological evidence to define a vitamin A deficiency cutoff using total liver vitamin A reserves

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 ?mol/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 ?mol/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 ?mol/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 ?mol/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.