Extract of Deschampsia antarctica (EDA) Prevents Dermal Cell Damage Induced by UV Radiation and 2,3,7,8-Tetrachlorodibenzo-p-dioxin.

Alicia Zamarrón,Concepción Parrado,Salvador González,Manuel Mataix,Silvia Rocío Lucena,Azahara Pérez-Davó,Esther Morel

doi:10.3390/ijms20061356

Alicia Zamarrón, Concepción Parrado + Show 5 more

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https://doi.org/10.3390/ijms20061356

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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.

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The skin is an organ specialized as a first major barrier against ionizing radiations and chemical damage
EDA does not have Apparent Effects on Healthy Fibroblasts and Keratinocytes, but Reverts Alterations Induced by UV Radiation
In order to study the potential protective properties of EDA against UV radiation, we first assessed whether EDA alters cell physiology on its own—in model skin cell cultures we studied in parallel human dermal fibroblasts and an established human keratinocyte cell line (HaCaT)

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The skin is an organ specialized as a first major barrier against ionizing radiations and chemical damage. Its complete exposure to environmental DNA damaging agents renders it susceptible of developing different pathologies, including cancer. Ultraviolet ionizing radiation (UVR) constitutes ~10% of total sunlight output, and is the most prominent causative factor for skin cancers (reviewed in open online resources: In. Ultraviolet Waves.; 2010). Its long- and medium-wave components A and B (UVA, wavelength 320–400 nm and UVB, wavelength 290–320 nm)—those most penetrant through the ozone layer—can induce DNA damage directly, by promoting the formation of specific DNA products (e.g., pyrimidine-pyrimidine dimers, most often formed by the crosslinking of thymine pairs). Surviving unrepaired damaged cells can initiate tumours or contribute to skin aging (reviewed in [2,3])

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