Glycation associated skin autofluorescence and skin elasticity are related to chronological age and body mass index of healthy subjects.

Glycation is the non-enzymatic reaction between reducing sugars and proteins that leads to the formation of advanced glycation end products (AGEs). In vivo skin autofluorescence (lambda(ex)/lambda(em)=370/440 nm) was used as a non-invasive clinical tool to study skin AGE accumulation in healthy panellists. Using multiple linear regression analysis, it was shown that for panellists below the age of 40, glycation associated in vivo skin fluorescence intensity increased as a function of chronological age and body mass index (BMI). Above the age of 40, the fluorescence was associated to age but not to BMI, suggesting that the effect of age became dominant over BMI. Since the accumulation of AGEs is expected to affect the biomechanical properties of the skin, in vivo skin elasticity data were gathered on a second panel. It was found that skin elasticity depended on age and BMI in a similar fashion as to what we observed for the skin fluorescence data. It is hypothesised that skin AGE accumulation contributes to the loss of skin elasticity in aged and/or overweight people.

Correlation between in vitro cyclic adenosine monophosphate phosphodiesterase inhibition and in vivo anti-inflammatory effect.

We tested the hypothesis that topical adenosine monophosphate phosphodiesterase (cAMP PDE) inhibitors are anti-inflammatory. These can be shown by a correlation between PDE inhibitory and anti-inflammatory function of a series of known PDE inhibitors. The effect of various cAMP PDE inhibitors on PDEs isolated from HaCaT cells was first investigated. These compounds were then tested as anti-irritants against topical 8% Balsam of Peru. A direct correlation was observed between the in vitro EC(50) values for PDE inhibition and the in vivo anti-inflammatory potential with a correlation coefficient of r = 0.79. These results stress the value of PDE inhibitors as anti-inflammatory agents in topical use, and also demonstrate that the in vitro PDE assay can be used to predict in vivo anti-inflammatory potential.

Protection against endogenous and UVB-induced oxidative damage in stratum corneum lipids by an antioxidant-containing cosmetic formulation.

A 16-week human clinical study was carried out to determine the ability of antioxidants in a cosmetic vehicle to inhibit the induction of lipid peroxidation in stratum corneum lipids. The study consisted of a twice daily application of material for 12 weeks followed by a 4-week regression phase. Stratum corneum lipids were collected and then exposed to 500 mJ/cm2 of ultraviolet B (UVB) radiation in order to avoid excessive erythemal damage to the subjects. Lipid peroxides were assayed by a methylene blue derivative assay and expressed per unit area of skin. During the treatment period, decreases in the level of lipid peroxides were observed on the sites treated with the compositions containing antioxidants, as compared to the untreated sites, and expressed as percent differences. Decreases were observed in endogenous as well as UV-induced lipid peroxides followed by a return to baseline levels. These results demonstrate that antioxidants in a topical cosmetic formulation were effective in protecting human stratum corneum lipids against endogenous oxidation or if challenged by 500 mJ/cm2 UVB.

Factors defining sensitive skin and its treatment.

BACKGROUND: Users of cosmetics and skin care products often report adverse reactions ranging from itching and dryness to intense inflammatory responses such as erythema or wheal and rash. Self-assessment is not always an accurate parameter for categorizing skin as sensitive or nonsensitive, although it can be valuable. For this reason, it is important to define sensitive skin by more objective factors. OBJECTIVE: Studies were undertaken to determine if objective biophysical measurements could detect differences in barrier function between those individuals who identified themselves as having sensitive skin and those self-identified as having normal skin. In addition, the effects of treatment on barrier functions of individuals with sensitive skin were determined. METHODS: Three main factors that contribute to cutaneous reactivities were observed for the estimation of skin sensitivity: barrier functions, reactivity to irritants, and neuronal responses manifested as sensory reactions. Barrier functions of the skin was tested by gentle removal of the stratum corneum with simple cellophane tape stripping followed by measurement of transepidermal water loss (TEWL) as a marker of barrier loss. The onset and intensity of skin reaction against an irritant, balsam of Peru, was tested on the same individuals to observe the reactivity of their skin. Using the lactic acid sting test, additional information regarding skin sensitivities was obtained. RESULTS: Sensitive skin individuals exhibiting easy barrier damage possess delicate skin that is also highly reactive to irritants. When these individuals used a regimen of products that contained minimal preservatives and no surfactants for 8 weeks, the skin barrier and reactivity changed such that it was similar to nonsensitive skin. CONCLUSIONS: Skin sensitivity is observed because of a combination of factors, including a disrupted barrier and a tendency to hyperreact to topical agents. Treatment with special topical skin care formulations can reduce overall skin sensitivity.

Effect of topical application of antioxidants and free radical scavengers on protection of hairless mouse skin exposed to chronic doses of ultraviolet B.

BACKGROUND/AIMS: Within the past three decades, there has emerged a greater awareness of the molecular effects of solar rays especially ultraviolet radiation (UV-R), to the extent that the harmful effects of solar radiation are recognized not only by molecular biologists and physicians, but also by the general public (1). Various sunscreen molecules that effectively block the UVB component of the sun are available; however, a large part of Western populations elicits adverse reactions against chemical sunscreens (2). This study was designed to observe the protective effect of antioxidants against the damaging effects of chronic UVB exposure of skin in an attempt to introduce antioxidants and free radical scavengers as topical sun protective agents. METHODS: Jackson hairless mice were exposed to suberythemal doses of UVB, three times a week, and topically treated with a cream containing the anti-oxidants vitamin E, butylated hydroxy-toluene, nordihydroguaradinic acid and vitamin C. RESULTS: Treatment with vehicle alone along with UVB exposure resulted in an increase in epidermal thickness showing a 38%, 77% and 112% increase after 4 weeks, 8 weeks and 12 weeks, respectively. Chronic UVB exposed skin treated with the material containing free radical scavengers and antioxidants mix (AO mix) exhibited 39%, 73% and 124% thicker epidermis than the un-treated control after, respectively, 4 weeks, 8 weeks and 12 weeks of treatment. The vehicle did not appear to protect skin against UV irradiation, since there appeared to be more (16%) sunburn cells in vehicle treated skin than the untreated, UV exposed skin after 4 weeks of treatment. After 8 weeks and 12 weeks, there were 33% and 36% less sunburn cells in the vehicle treated skin than the untreated, UV exposed skin. The antioxidant mix was significantly effective (P=<0.001) in protecting against UVB irradiation, having 63%, 71 % and 79% fewer sunburn cells than the untreated, UV exposed skin after 4 weeks, 8 weeks and 12 weeks of treatment, respectively. CONCLUSION: Data from these studies suggest that low level chronic exposures to UV can lead to alteration of the skin, like epidermal thickening and appearance of sunburn cells. The data also indicates that a mix of common antioxidants and free radical scavengers are photoprotective against chronic skin damage in the hairless mouse skin model.