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Due to changes in human lifestyle (expanded sunbathing, the use of solaria, etc.) and, most importantly, increasing lifetime and thus higher cumulative exposure to solar radiation, skin aging and skin cancer have become major health issues. As a consequence effective photoprotection is of outmost importance to humans. In this regard a lot has been learned in the past about the cellular and molecular basis underlying ultraviolet (UV) radiation-induced skin damage and, based on this knowledge, numerous skin protective approaches including organic and inorganic UV-filters, but also topically applicable antioxidants, DNA repair enzymes and compatible solutes as well as oral photoprotective strategies based on nutritional supplements have been developed. A new aspect is here that sun protection of human skin might even be possible after solar radiation-induced skin damage has occurred. A second, very important development was prompted by the discovery that also wavelengths beyond the UV spectrum can damage human skin. These include the blue light region of visible light (VIS) as well as the near infrared range (IRA) and corresponding sunprotection strategies have thus recently been or are still being developed. In this article we will provide a state of the art summary of these two novel developments and, at the end, we will also critically discuss strengths and weaknesses of the current attempts, which mainly focus on the prevention of skin damage by selected wavelengths but greatly ignore the possibility that wavelengths might interfere with each other. Such combined effects, however, need to be taken into account if photoprotection of human skin is intended to be global in nature.

Ultraviolet B (UVB) radiation induces mutagenic DNA photoproducts, in particular cyclobutane pyrimidine dimers (CPDs), in epidermal keratinocytes (KC). To prevent skin carcinogenesis, these DNA photoproducts must be removed by nucleotide excision repair (NER) or apoptosis. Here we report that the UVB-sensitive transcription factor aryl hydrocarbon receptor (AHR) attenuates the clearance of UVB-induced CPDs in human HaCaT KC and skin from SKH-1 hairless mice. Subsequent RNA interference and inhibitor studies in KC revealed that AHR specifically suppresses global genome but not transcription-coupled NER. In further experiments, we found that the accelerated repair of CPDs in AHR-compromised KC depended on a modulation of the p27 tumor suppressor protein. Accordingly, p27 protein levels were increased in AHR-silenced KC and skin biopsies from AHR −/− mice, and critical for the improvement of NER. Besides increasing NER activity, AHR inhibition was accompanied by an enhanced occurrence of DNA double-strand breaks triggering KC apoptosis at later time points after irradiation. The UVB-activated AHR thus acts as a negative regulator of both early defense systems against carcinogenesis, NER and apoptosis, implying that it exhibits tumorigenic functions in UVB-exposed skin. In fact, AHR −/− mice developed 50% less UVB-induced cutaneous squamous cell carcinomas in a chronic photocarcinogenesis study than their AHR +/+ littermates. Taken together, our data reveal that AHR influences DNA damage-dependent responses in UVB-irradiated KC and critically contributes to skin photocarcinogenesis in mice.

There is a continuing interest in whether Bisphenol A (BPA) is able to cause adverse health effects through interaction with elements of the immune system. That interest has been fuelled further by the recent publication of a draft opinion on BPA prepared by the European Food Safety Authority (EFSA) Panel on Food Contact Materials, Enzymes and Processing Aids (CEP). This draft opinion judged effects on the immune system to be the most sensitive health outcome, and identified BPA-induced changes in the frequency of T-helper (T H )-17 cells in the spleens of mice as being the critical effect based on an association of these cells with inflammation. Based on these evaluations the CEP Panel recommended that a revised Tolerable Daily Intake (TDI) for BPA of 0.04 ng/kg bw/day should be adopted; representing a very substantial reduction (100,000-fold) compared with the existing TDI. The purpose of this commentary is to summarize briefly the role of T H 17 cells in immune responses, and to review relevant literature regarding the influence of BPA on these cells, and on inflammatory responses in the lung and respiratory allergy. The conclusion drawn is that based on uncertainties about the effects of BPA on T H 17 cells and lung inflammation in mice, the absence of consistent or persuasive evidence from human studies that exposure of BPA is associated with inflammation or allergy, and unresolved questions regarding the species selectivity of immune effects induced by BPA, it is inappropriate to adopt the revised TDI. Additional research is required to explore further the influence of BPA on the immune system and immune responses.

There is a continuing interest in whether Bisphenol A (BPA) is able to cause adverse health effects through interaction with elements of the immune system. That interest has been fuelled further by the recent publication of a draft opinion on BPA prepared by the European Food Safety Authority (EFSA) Panel on Food Contact Materials, Enzymes and Processing Aids (CEP). This draft opinion judged effects on the immune system to be the most sensitive health outcome, and identified BPA-induced changes in the frequency of T-helper (T )-17 cells in the spleens of mice as being the critical effect based on an association of these cells with inflammation. Based on these evaluations the CEP Panel recommended that a revised Tolerable Daily Intake (TDI) for BPA of 0.04 ng/kg bw/day should be adopted; representing a very substantial reduction (100,000-fold) compared with the existing TDI. The purpose of this commentary is to summarize briefly the role of T 17 cells in immune responses, and to review relevant literature regarding the influence of BPA on these cells, and on inflammatory responses in the lung and respiratory allergy. The conclusion drawn is that based on uncertainties about the effects of BPA on T 17 cells and lung inflammation in mice, the absence of consistent or persuasive evidence from human studies that exposure of BPA is associated with inflammation or allergy, and unresolved questions regarding the species selectivity of immune effects induced by BPA, it is inappropriate to adopt the revised TDI. Additional research is required to explore further the influence of BPA on the immune system and immune responses.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.An amendment to this paper has been published and can be accessed via a link at the top of the paper.