BackgroundPhotoprotection of human skin is determined as the capacity of sunscreens to prevent ultraviolet (UV) B radiation‐induced erythema and UVA radiation‐induced pigmentation. It is unequivocal that, in addition to sunscreens, oral supplementation with carotenoids can protect human skin against UVB radiation‐induced erythema. It is not known if this is also the case for UVA radiation‐induced pigmentation.ObjectiveTo clinically evaluate the photoprotective effects of daily supplementation with carotenoids against UVA radiation‐induced pigmentation.MethodsIn this double‐blind, placebo‐controlled trial, 60 subjects (Fitzpatrick types II‐IV) were randomized to receive Nutrilite™ Multi Carotene supplement or placebo for 12 weeks. UVB‐induced minimal erythemal dose (MED), UVA‐induced minimal persistent pigmentation dose (MPPD) and skin carotenoid levels were measured at baseline, 4, 8, and 12 weeks of intervention. Skin color was evaluated by expert clinical graders and by colorimetry. Carotenoid levels in the skin were measured by the Biozoom® device.ResultsIn the intervention group, a significant increase in comparison with the placebo group was observed in (a) skin carotenoid levels, (b) UVB‐induced MED, and (c) UVA‐induced MPPD values obtained by colorimetry.ConclusionDaily supplementation with carotenoids protects human skin against both UVB‐induced erythema and UVA‐induced pigmentation.
Summary
Background
Melanocytes, which reside in the basal layer of the epidermis, produce the pigment melanin in cytoplasmic organelles known as melanosomes. Melanosomes are transferred to keratinocytes which provide the color in our skin. Recently, Diwakar et al reported the crucial roles of protein glycosylation in both melanogenesis and melanosome transfer to keratinocytes, and each was inhibited by the nucleotide cytidine.
Objective
The main objective of this study was to determine the clinical effects of topical application of cytidine to the hyperpigmented regions of the face in a group of human volunteers.
Methods
A randomized, vehicle‐controlled study was conducted for 12 weeks on healthy Korean female subjects. Cytidine was formulated into the lotion at concentrations of 2%, 3%, and 4% (w/w) and compared to the vehicle control formulation. The clinical outcomes were evaluated by performing visual assessment grading, measuring melanin index, skin brightness, and skin color parameters. In vitro skin penetration studies were conducted using Franz cell chambers for the 2% cytidine test formulation.
Results
The test group showed significant improvements in the visual assessment scores, melanin index, skin brightness, and skin color compared to the control group. Although significant dose‐dependent improvements were seen in the clinical study, the in vitro Franz cell studies indicated that the clinical efficacy and potency of cytidine might be further enhanced by formulating a better topical delivery system, which will be the goal of our future studies.
Conclusions
This randomized, double‐blind, 12‐week clinical study successfully demonstrated the efficacy of cytidine on skin depigmentation in a dose‐dependent manner.
There is an increasing awareness that environmental factors, such as UV radiation, cigarette smoke, smog, industrial pollution, have negative impacts on skin and lead to premature aging, and in some case even skin cancer. Previous studies have shown that one of the negative actions from UV radiation is to cause DNA damage, such as cyclobutane pyrimidine dimers (CPD). Nucleotide excision repair (NER) has been shown to be critical for the repair of CPDs, and the excision repair cross-complementation group1 (ERCC1) has been found to be one of the rate-limiting enzymes in the NER pathway. Keratinocyte specific deletion of ERCC1 in mice causes hypersensitivity to UV-induced skin cancer, demonstrating the critical role of ERCC1 in repairing UV-induced DNA damage. However, ERCC1 has been shown to be down-regulated during aging process, potentially reducing the body's ability to repair CPDs through NER over time. In an effort to mitigate the reduction of ERCC1 expression and the resultant diminution of the body's potential to repair skin DNA damage caused by UV through NER, we initiated a screening program to identify technologies that enhance ERCC1 expression in 3D skin equivalent tissues in vitro. In this presentation, we report on the identification of novel technologies that were able to increase ERCC1 to enhance the DNA repair potential, thereby reducing DNA damage caused by UV radiation in 3D skin equivalent in vitro.
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