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Retinyl Palmitate
Published in Anton C. de Groot, Monographs in Contact Allergy, 2021
Retinyl palmitate is a naturally occurring phenyl analog of retinol (vitamin A) with potential antineoplastic and chemopreventive activities. As the most common form of vitamin A taken for dietary supplementation, retinyl palmitate binds to and activates retinoid receptors, thereby inducing cell differentiation and decreasing cell proliferation. This agent also inhibits carcinogen-induced neoplastic transformation, induces apoptosis in some cancer cell types, and exhibits immunomodulatory properties. Retinyl palmitate is a common vitamin supplement, available in both oral and injectable forms for treatment of vitamin A deficiency. In cosmetics it may be used as skin conditioning agent (1).
Methods for in Vitro Skin Metabolism Studies
Published in Francis N. Marzulli, Howard I. Maibach, Dermatotoxicology Methods: The Laboratory Worker’s Vade Mecum, 2019
The absorption and metabolism of retinyl palmitate were measured to see if ester hydrolysis and alcohol oxidation occurred with this cosmetic ingredient (Table 3). Skin absorption for this lipophilic material is the sum of the absorbed compound in skin and the compound present in the receptor fluid at the end of the 24-h study. Most of the absorbed radioactivity remained in the skin. Substantial amounts of the absorbed compound were hydrolyzed to retinol, but no oxidation of the alcohol to retinoic acid was observed. Any effects of retinyl palmitate on the structure of skin may be due to the formation of retinol during percutaneous absorption.
Treatment of skin with antioxidants
Published in Roger L. McMullen, Antioxidants and the Skin, 2018
Retinoids are commonly used to treat acne vulgaris or photodamaged skin. Topical treatment is normally achieved with retinol, retinal, or retinyl esters (e.g., retinyl palmitate).51 By enzymatic activity, these molecules are converted in skin to the active form, trans-retinoic acid. Most of present knowledge of the mechanism and function of trans-retinoic acid in skin deals with the epidermis.52 It binds to retinoic acid and retinoid X receptors, triggering a series of biochemical events and ultimately stimulating keratinocyte proliferation and increasing the thickness of the epidermal layer. In addition, retinoids affect the dermis by such action on fibroblasts as the down regulation of collagenase, an enzyme that breaks down peptide bonds in collagen, which would ultimately lead to damaged structural collagen fibrils in the dermis and alteration of skin mechanical properties and visual aesthetics.53
Early changes in the immune microenvironment of oral potentially malignant disorders reveal an unexpected association of M2 macrophages with oral cancer free survival
Published in OncoImmunology, 2021
Jebrane Bouaoud, Jean-Philippe Foy, Antonin Tortereau, Lucas Michon, Vincent Lavergne, Nicolas Gadot, Sandrine Boyault, Julie Valantin, Geneviève De Souza, Philippe Zrounba, Chloé Bertolus, Nathalie Bendriss-Vermare, Pierre Saintigny
We have evaluated the association of some M2 macrophages gene expression signatures with Oral Cancer Free Survival (OCFS) using data previously published from 86 patients with OPMD, in particular, oral leukoplakia15 (GSE26549) (Supplementary Table 6). Briefly, gene expression profile was measured in 86 Oral leukoplakia patients who were enrolled in a clinical chemoprevention trial that used the incidence of oral cancer development as a prespecified endpoint.16 After inclusion, the patients were randomly assigned to intervention (13-cis- retinoic acid versus retinyl palmitate with or without beta-carotene). OCFS was defined as the time from random assignment until diagnosis of any OSCC. Analysis of OCFS was performed in the entire intent-to-treat population and was analyzed by the Kaplan-Meier method. The median follow-up time was 7.11 years and 35 of the 86 patients developed oral cancer over the course. The average time between the OL and OSCC diagnosis is 3.11 years (0.18–14.33).
Differential effect of a carotenoid-rich diet on retina function in non-diabetic and diabetic rats
Published in Nutritional Neuroscience, 2020
Kathleen J. McClinton, Michel Aliani, Sharee Kuny, Yves Sauvé, Miyoung Suh
Since liver is the primary storage site, and regulator of vitamin A homeostasis, liver retinoid and carotenoid concentrations (µg/g liver) were measured to determine the effects of carrot supplementation in non-diabetic control and diabetic rats (Figure 4). Rats fed the carrot supplemented diet had significantly (p < 0.04) higher retinol and retinyl palmitate concentrations in both control and diabetic groups. Carrot enrichment led to the highest levels of liver retinol and retinyl palmitate reserves in non-diabetic control rats, with 1.3 and 3.4 fold increases, respectively, compared with smaller increases in diabetic rats, 1.1 and 1.6 folds, respectively. Diabetic compared with non-diabetic rats, had lower liver concentrations of retinol and retinyl palmitate (p < 0.005). Retinol was decreased by 36% and 35%, and retinyl palmitate was decreased by 23% and 48%, for control and carrot fed group, respectively.
Microencapsulation of retinyl palmitate by melt dispersion for cosmetic application
Published in Journal of Microencapsulation, 2020
Aditi Nandy, Eliza Lee, Abhyuday Mandal, Raha Saremi, Suraj Sharma
Retinyl palmitate (RP) (C36H60O2), is a stable lipophilic ester of retinol and palmitic acid. Although pure retinol is more effective in anti-aging than its derivatives, it has adverse effects such as burning, redness, and peeling off the skin. On the contrary, RP has a mild and slow reaction on the skin. After being topically applied onto the skin, RP needs to be converted to retinol catalysed by enzymes within the skin, and then to active retinoic acid through oxidative processes (Boerman and Napoli 1996, Lupo 2001, Oliveira 2014). Figure 1(b) shows the schematic of this mechanism. However, there is evidence of the effectiveness of RP as antiaging in previous studies. A study by Counts et al. (1988) showed that topical administration of RP in rats for 14 days resulted in an epidermal thickening with enhanced protein and collagen stimulation. In another comparison study (Duell et al.1997), an increased epidermal thickness was observed in human skin as well.