The skin is the main barrier that protects us against environmental stressors (physical, chemical, and biological). These stressors, combined with internal factors, are responsible for cutaneous aging. Furthermore, they negatively affect the skin and increase the risk of cutaneous diseases, particularly skin cancer. This review addresses the impact of environmental stressors on skin aging, especially those related to general and specific external factors (lifestyle, occupation, pollutants, and light exposure). More specifically, we have evaluated ambient air pollution, household air pollutants from non-combustion sources, and exposure to light (ultraviolet radiation and blue and red light). We approach the molecular pathways involved in skin aging and pathology as a result of exposure to these external environmental stressors. Finally, we reflect on how components of environmental stress can interact with ultraviolet radiation to cause cell damage and the critical importance of knowing the mechanisms to develop new therapies to maintain the skin without damage in old age and to repair its diseases.

Skin is being increasingly exposed to artificial blue light due to the extensive use of electronic devices. This, together with recent observations reporting that blue light—also known as high-energy visible light—can exert cytotoxic effects associated with oxidative stress and promote hyperpigmentation, has sparked interest in blue light and its potential harmful effects on skin. The photoprotective properties of new extracts of different botanicals with antioxidant activity are therefore being studied. Deschampsia antarctica (Edafence^®, EDA), a natural aqueous extract, has shown keratinocyte and fibroblast cell protection effects against ultraviolet radiation and dioxin toxicity. In this regard, we studied the protective capacity of EDA against the deleterious effects of artificial blue light irradiation in human dermal fibroblasts (HDF) and melanocytes. We analyzed the impact of EDA on viability, cell morphology, oxidative stress, melanogenic signaling pathway activation and hyperpigmentation in HDF and melanocytes subjected to artificial blue light irradiation. Our results show that EDA protects against cell damage caused by artificial blue light, decreasing oxidative stress, melanogenic signaling pathway activation and hyperpigmentation caused by blue light irradiation. All these findings suggest that EDA might help prevent skin damage produced by artificial blue light exposure from screen of electronic devices.

Exposure to natural and artificial light and environmental pollutants are the main factors that challenge skin homeostasis, promoting aging or even different forms of skin cancer through a variety of mechanisms that include accumulation of reactive oxygen species (ROS), engagement of DNA damage responses, and extracellular matrix (ECM) remodeling upon release of metalloproteases (MMPs). Ultraviolet A radiation is the predominant component of sunlight causative of photoaging, while ultraviolet B light is considered a potentiator of photoaging. In addition, different chemicals contribute to skin aging upon penetration through skin barrier disruption or hair follicles, aryl hydrocarbon receptors (AhR) being a major effector mechanism through which toxicity is exerted. Deschampsia antarctica is a polyextremophile Gramineae capable of thriving under extreme environmental conditions. Its aqueous extract (EDA) exhibits anti- photoaging in human skin cells, such as inhibition of MMPs, directly associated with extrinsic aging. EDA prevents cellular damage, attenuating stress responses such as autophagy and reducing cellular death induced by UV. We demonstrate that EDA also protects from dioxin-induced nuclear translocation of AhR and increases the production of loricrin, a marker of homeostasis in differentiated keratinocytes. Thus, our observations suggest a potential use exploiting EDA’s protective properties in skin health supplements.

An extremely halophilic archaeon, strain S2FP14^T, was isolated from a brine sample from the inland hypersaline lake Fuente de Piedra, a saline-wetland wildfowl reserve located in the province of Málaga in southern Spain. Colonies were red-pigmented and the cells were Gram-staining-negative, motile and pleomorphic. S2FP14^T was able to grow in media containing 12.5–30 % (w/v) total salts (optimum 20 %) at pH 7–8.5 (optimum 7.5) and at 25–50 °C (optimum 37 °C). The 16S rRNA gene sequence analysis indicated that this strain represented a member of the genus Halobellus. S2FP14^T showed a similarity of 99.5 % to Halobellus inordinatus YC20^T, 96.1 % to Halobellus litoreus GX31^T, 95.9 % to Halobellus limi TBN53^T, 95.5 % to Halobellus rarus YC21^T, 95.2 % to Halobellus rufus CBA1103^T, 94.6 % to Halobellus salinus CSW2.24.4^T and 94.6 % to Halobellus clavatus TNN18^T. The rpoB′ gene sequence similarity of strain S2FP14^T was 97.4 % to 87.6 % with members of genus Halobellus. The major phospholipids of strain S2FP14^T were phosphatidylglycerol phosphate methyl ester and phosphatidylglycerosulfate, plus a very small amount of phosphatidylglycerol and an archaeal analogue of bisphosphatidylglycerol. With regard to glycolipid composition, the most abundant glycolipids were the sulfated diglycosyl diphytanilglyceroldiether and a glycosyl-cardiolipin. The G+C content of strain S2FP14^T genomic DNA was 61.4 mol%. The DNA–DNA hybridization between strain S2FP14^T and Halobellus inordinatus JCM 18361^T was 51 %. Based on the phylogenetic, phenotypic and chemotaxonomic features, a novel species, Halobellus ramosii sp. nov. is proposed. The type strain is S2FP14^T ( = CECT 8167^T = DSM 26177^T).