An important step towards the comprehensive sun protection: Blue-light exposure inhibits DNA repair in reconstituted human skin and a broadband sunscreen avoids this inhibition.

The field of sun protection is quickly changing and the research article by Douki et al., published in the current issue of Photochemistry and Photobiology, reported key experimental data that will certainly help the development of better sun care products. Mutagenic photoproducts (CPDs, cyclobutane pyrimidine dimers and 6-4PPs, pyrimidine-6-4-pyrimidone photoproducts) were formed in the reconstructed human epidermis (RHE) by UVB (312 nm) irradiation, and their concentrations were detected by HPLC-MS/MS as a function of time after the UVB treatment.

The phototoxicity action spectra of visible light in HaCaT keratinocytes.

Visible light (VL) surely affects human skin in several ways, exerting positive (tissue regeneration, pain relief) and negative (oxidation, inflammation) effects, depending on the radiation dose and wavelength. Nevertheless, VL continues to be largely disregarded in photoprotection strategies, perhaps because the molecular mechanisms occurring during the interaction of VL with endogenous photosensitizers (ePS) and the subsequent biological responses are still poorly understood. Besides, VL encompass photons with different properties and interaction capacities with the ePS, but there are no quantitative comparisons of their effects on humans.

[Historical construction of the concept of the enzyme and approaches in biology textbooks].

The use of the history and philosophy of science in teaching and learning is commonly neglected, linear, and/or out of context in textbooks. This article investigates whether this also occurs with the concept of enzymes. A brief review of the literature establishes the theoretical foundation to investigate how the concept of enzymes is presented in nine textbooks, following three different lines of analysis.

Lipofuscin in keratinocytes: Production, properties, and consequences of the photosensitization with visible light.

A dysfunction in the mitochondrial-lysosomal axis of cellular homeostasis is proposed to cause cells to age quicker and to accumulate lipofuscin. Typical protocols to mediate lipofuscinogenesis are based on the induction of the senescent phenotype either by allowing many consecutive cycles of cell division or by treating cells with physical/chemical agents such as ultraviolet (UV) light or hydrogen peroxide. Due to a direct connection with the physiopathology of age-related macular degeneration, lipofuscin that accumulates in retinal pigment epithelium (RPE) cells have been extensively studied, and the photochemical properties of RPE lipofuscin are considered as standard for this pigment.