Visible light (400-700nm), which contributes to 45% of solar radiation, contributes to skin darkening and worsening of dyschromias, particularly in individuals with Fitzpatrick skin phototypes III and higher. Currently, sunscreens provide limited protection against that spectrum. Due to their capabilities in absorbing, scattering, and reflecting visible light, topical products containing pigments and/or metal oxides can provide additional photoprotection. In this study, the efficacy of two formulations containing iron oxide was evaluated in preventing visible light-induced pigmentation compared with a non-tinted mineral SPF 50+ sunscreen. Expert grading and colorimetry demonstrated that the iron-oxide containing formulations significantly protected against visible light-induced pigmentation compared to untreated skin or mineral SPF 50+ sunscreen in Fitzpatrick IV individuals. These results highlight that iron-oxide containing formulas in a foundation format have dual functions and can provide additional benefits in patients' daily routine by masking existing pigmentation and preventing the development of pigmentation triggered by sunlight exposure, extending protection beyond UV spectrum.

Given its properties and efficacy in cancer killing, our results suggest that OBT is a promising cancer therapeutic.

Exposure to high doses of solar long wavelength ultraviolet radiation (UVA) damages human skin via reactive oxygen species (ROS). Whether physiological UVA doses also generate ROS that has an effect on the skin remains unknown. We previously showed that in human epidermal melanocytes UVA activates a G‐protein coupled signaling pathway that leads to calcium mobilization and increased melanin. Here, we report that ROS generated by the UVA phototransduction pathway are critical cellular messengers required to augment melanin. Using simultaneous UVA exposure and live‐cell imaging of primary human melanocytes, we found that physiological doses of UVA generate two spatiotemporally distinct sources of ROS: one upstream of the G‐protein activation that potentiates calcium responses, and another source downstream of calcium, in the mitochondria (ROSmito). UVA‐evoked signaling led to mitochondrial calcium uptake via mitochondrial calcium uniporter to promote ROSmito production leading to melanin synthesis. Our findings reveal a novel mechanism in which ROS function as signaling messengers necessary for melanin production, thus having a protective role in the UVA‐induced skin response.

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