Oxidative stress is an integral element that influences a variety of biochemical reactions throughout the body and is known to play a notable role in melanogenesis. Exogenous triggers of oxidative stress, such as ultraviolet radiation (UVR) and visible light (VL), lead to pigment formation through somewhat different pathways, but both share a common endpoint-the potential to generate cosmetically undesirable hyperpigmentation. Though organic and inorganic sunscreens are available to protect against the UVR portion of the electromagnetic spectrum, coverage is lacking to protect against the VL spectrum. In this manuscript, we review the phases of tanning, pathways of melanogenesis triggered by UVR and VL, and the associated impact of oxidative stress. We also discuss the known intrinsic mechanisms and paracrine regulation of melanocytes that influence their response to UVR. Understanding these mechanisms and their role in UVR-induced hyperpigmentation should potentially lead to identification of useful targets that can be coupled with antioxidant therapy to alleviate this effect.

The role of topical antioxidants (AOs) on visible light plus ultraviolet A1 (VL+UVA1)-induced skin changes were evaluated. Twenty subjects with skin phototypes (SPTs) I-VI had placebo and concentrations of an AO blend applied to their back (AO 0.5%, 1.0% and 2.0%). Treated and control sites were irradiated with VL+UVA1. Colorimetric and diffuse reflectance spectroscopy (DRS) assessments were performed immediately, 24 h and 7 days after irradiation. Subjects with SPT I-III had erythema that faded within 24 h, while SPT IV-VI had persistent pigmentation. SPT I-III demonstrated significantly less erythema at the 2% AO site while SPT IV-VI demonstrated significantly less immediate pigmentation at 2% AO site and less pigmentation (approaching significance, P = 0.07) on day 7 compared with control. Immunohistochemistry from biopsies of 2% AO and placebo at 24 h did not demonstrate a significant change in COX-2 or MART-1 for any SPT. There was a decrease in cyclin D1 for SPT IV-VI which was approaching significance (P = 0.06) but not for SPT I-III. The results indicate that topical AO inhibits erythema in SPT I-III and reduces pigmentation in SPT IV-VI caused by VL+UVA1. AO may help prevent worsening of pigmentary disorders and should be incorporated into photoprotection.

Solar radiation is a major contributor to the development of skin cancer. Recent studies have shown that visible light (VL), a major portion of solar spectrum, induces biologic effects on the skin. Ultraviolet filters in currently available broad‐spectrum sunscreens do not offer protection against VL. This study was designed to identify the spectral characteristics of the skin responses induced by VL, which can be utilized for time efficient in vivo VL testing. Thirty‐one subjects were irradiated with a light source emitting visible light with less than 0.5% long wavelength UVA1 (VL + UVA1, 370‐700 nm), and 41 subjects were irradiated with pure visible light (pure VL, 400‐700 nm). Assessments including clinical photography, investigator's global assessment of pigmentation and erythema, and diffuse reflectance spectroscopy (DRS) performed immediately and seven days after irradiation. Clinical and spectroscopic data showed that VL + UVA1 spectral output induced significantly darker and persistent skin responses as compared to those induced by pure VL. Spectroscopic signatures of skin responses induced by both radiation sources were identified. The signatures were found to be specific to the radiation source and time of collection. A method to evaluate VL protection factor, using quantitative information from the spectral signatures obtained, was proposed.

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