|
|
|
|
|
Topically Applied Vitamin A Increases the Thickness of the EpidermisOn this page we look at how topically applied Vitamin A increases the thickness of the epidermis. With aging, the epidermis tends to thin, leading to a thin and fragile skin - prone to wrinkling and premature aging. A thickening effect of the skin, has some very valid anti-aging effects. The tests were all done on human skin as well as mice, and shows conclusively that topical application of vitamin A to the skin has a thickening effect on the skin.
Vitamin A (in sesame oil) applied topically to the skin for 10 days caused an average increase in epidermal thickness to about twice normal. A notable increase in the extent of the stratum granulosum occurred, and a decreased rate of keratin formation and possible increased rate of keratohyalin formation are suggested. The effect was apparently entirely local. Estradiol benzoate, similarly applied, caused no observable change in the epidermis and did not counteract the stimulatory effect of the vitamin.
We investigated the clinical, histologic, and molecular responses of normal human skin to all-trans-retinol (ROL) application, compared to those induced by topical all-trans-retinoic acid (RA), and measured ROL-derived metabolites. Up to 1.6% ROL, 0.025% RA in vehicle (70% ethanol/30% propylene glycol), or vehicle alone were applied in a double-blind fashion to normal buttock skin and occluded for 4 days. ROL produced from none to only trace erythema, which was clinically and statistically insignificant, whereas RA induced a significant 3.7-fold increase in erythema score compared to vehicle (n = 10, p < 0.01). However, ROL induced significant epidermal thickening (1.5-fold at 1.6% ROL, p < 0.01), similar to RA (1.6-fold at 0.025% RA, p < 0.01), relative to the vehicle. ROL, compared with vehicle, also increased mRNA levels of cellular retinoic acid binding protein (CRABP-II) and cellular retinol binding protein (CRBP) genes as determined by Northern analysis (5-6-fold and 6-7-fold, respectively) and riboprobe in situ hybridization. CRABP-II and CRBP protein levels were also higher following ROL than vehicle treatment, as measured by ligand binding (3.2-fold, p < 0.001; n = 7) and Western analysis (3.6-fold, p < 0.003; n = 6), respectively. Epidermal retinyl ester (RE) content, measured after removal of stratum corneum, rose 240-fold (p < 0.005, n = 5) by 24 h of ROL occlusion. RA content, however, was undetectable or detectable only at trace amounts in all samples obtained at 0, 6, 24, and 96 h after ROL occlusion. Detectability of RA was not correlated with ROL treatment (compared to untreated normal skin, p = 0.86) or baseline skin ROL levels (average r = -0.1, p > 0.3). These data demonstrate that ROL application 1) produces trace erythema not significantly different from vehicle, whereas RA causes erythema; 2) induces epidermal thickening and enhances expression of CRABP-II and CRBP mRNAs and proteins as does RA; 3) causes marked accumulation of retinyl ester; and 4) does not significantly increase RA levels. Taken together, the data are compatible with the idea that ROL may be a prohormone of RA, because it produces changes in skin similar to those produced by RA but without measurable RA or irritation.
Vitamin A in our skin care products |
|
PLEASE NOTE: Although we quote some animal studies, we at Dermaxime do NOT test any of our products on animals. For more on animal testing and our stand on this, please click here. |
|
|
|
