Natural Antioxidants: Multiple Mechanisms to Protect Skin From Solar Radiation

Abstract

Human skin exposed to solar ultraviolet radiation (UVR) results in a dramatic increase in the production of reactive oxygen species (ROS). The sudden increase in ROS shifts the natural balance toward a pro-oxidative state, resulting in oxidative stress. The detrimental effects of oxidative stress occur through multiple mechanisms that involve alterations to proteins and lipids, induction of inflammation, immunosuppression, DNA damage, and activation of signaling pathways that affect gene transcription, cell cycle, proliferation, and apoptosis. All of these alterations promote carcinogenesis and therefore, regulation of ROS levels is critical to the maintenance of normal skin homeostasis. Several botanical products have been found to exhibit potent antioxidant capacity and the ability to counteract UV-induced insults to the skin. These natural products exert their beneficial effects through multiple pathways, including some known to be negatively affected by solar UVR. Aging of the skin is also accelerated by UVR exposure, in particular UVA rays that penetrate deep into the epidermis and the dermis where it causes the degradation of collagen and elastin fibers via oxidative stress and activation of matrix metalloproteinases (MMPs). Because natural compounds are capable of attenuating some of the UV-induced aging effects in the skin, increased attention has been generated in the area of cosmetic sciences. The focus of this review is to cover the most prominent phytoproducts with potential to mitigate the deleterious effects of solar UVR and suitability for use in topical application.

Keywords: antioxidants; inflammation; oxidative stress; reactive oxygen species; skin cancer; ultraviolet radiation.

Figure 1

Effects of solar ultraviolet radiation in skin. Simplified representation of the effects of UVR (UVA+UVB) in epidermal keratinocytes. Exposure to UVR induces the formation of reactive oxygen species (ROS). Increase in ROS causes the imbalance between pro-oxidants and anti-oxidants, generating oxidative stress, which in turn, damages lipids, proteins, and DNA. Increases in ROS leads to the imbalance between pro-oxidants and anti-oxidants, generating oxidative stress, which in turn, damages lipids and proteins. Oxidative stress also leads to DNA damage which is compounded by the direct DNA damage known to be produced by UVB. ROS causes the activation of transcription factors such as Nrf2, JNK, and NF-kB. These transcription factors will bind to their specific DNA sequences, antioxidant responsive element (ARE), AP-1 (c-Fos/c-Jun), and NF-kB, respectively. Among the downstream targets of these transcription factors are the phase II antioxidants, and genes associated to promotion of cell proliferation and synthesis of pro-inflammatory mediators (i.e., COX-2, prostaglandin E2, interleukins). Inflammation causes edema, erythema in addition to further increase ROS formation. ROS-induced alteration to lipids and proteins lead to abnormal cellular signaling potentially promoting carcinogenesis. In addition, oxidative stress causes the synthesis and release of matrix metalloproteinases (MMPs) that degrade collagen, a biomarker of skin aging.