The Damaging Effects of Long UVA (UVA1) Rays: A Major Challenge to Preserve Skin Health and Integrity

Abstract

Within solar ultraviolet (UV) light, the longest UVA1 wavelengths, with significant and relatively constant levels all year round and large penetration properties, produce effects in all cutaneous layers. Their effects, mediated by numerous endogenous chromophores, primarily involve the generation of reactive oxygen species (ROS). The resulting oxidative stress is the major mode of action of UVA1, responsible for lipid peroxidation, protein carbonylation, DNA lesions and subsequent intracellular signaling cascades. These molecular changes lead to mutations, apoptosis, dermis remodeling, inflammatory reactions and abnormal immune responses. The altered biological functions contribute to clinical consequences such as hyperpigmentation, inflammation, photoimmunosuppression, sun allergies, photoaging and photocancers. Such harmful impacts have also been reported after the use of UVA1 phototherapy or tanning beds. Furthermore, other external aggressors, such as pollutants and visible light (Vis), were shown to induce independent, cumulative and synergistic effects with UVA1 rays. In this review, we synthetize the biological and clinical effects of UVA1 and the complementary effects of UVA1 with pollutants or Vis. The identified deleterious biological impact of UVA1 contributing to clinical consequences, combined with the predominance of UVA1 rays in solar UV radiation, constitute a solid rational for the need for a broad photoprotection, including UVA1 up to 400 nm.

The Safety and Efficacy of 1-Monoeicosapentaenoin Isolated from the Trebouxiophyceae Micractinium on Anti-Wrinkle: A Split-Face Randomized, Double-Blind Placebo-Controlled Clinical Study

“…On the other hand, other groups reported that the UVB are mostly responsible for skin changes such as wrinkle formation, epidermal thickening, degradation of matrix macromolecules, vascularization, and immunosuppression. However, UVA is partly absorbed and has lower efficiency in skin damage such as erythema [ 25 , 26 , 27 ]. In addition, previous studies reported that high-dose UVB irradiation led to apoptotic (e.g., sunburn) [ 28 , 29 , 30 ] or cancerous phenotypes [ 31 , 32 ] in skin, while low-dose UVB exposure accelerated skin aging or photoaging [ 1 ].…”

Oxidative Stress and Phototherapy in Atopic Dermatitis: Mechanisms, Role, and Future Perspectives

“…Despite their low energetic properties, the biological impact of UVA1 on human skin is not negligible because of their penetration properties and the OS that they are able to induce on a massive scale, thus affecting the skin as a whole [ 87 ]. In their recent review, Bernerd et al highlight the role of NRF2 in partially counteracting UVA1-induced OS through upregulation of NRF2 target genes: heme oxygenase 1 gene (HMOX1), thioredoxin reductase 1 (TXNRD1), NAD(P)H quinone dehydrogenase 1 (NQO1), ferritin light chain (FTL), glutamate-cysteine ligase regulatory subunit (GCLM), aldo-keto reductases 2/3 (AKR1C2 and AKR1C3), showing the validity of such involvement both in vivo and in a three-dimensional reconstructed human skin model [ 88 ]. Interestingly, the same defense mechanisms induced by OS in the dermis and completely differentiated epidermis also concern cancer cells, suggesting in this sense a multi-cytotype protective role of the NRF2 pathway in coping with the photoinduced OS.…”

Post-Translational Modifications Evoked by Reactive Carbonyl Species in Ultraviolet-A-Exposed Skin: Implication in Fibroblast Senescence and Skin Photoaging

“…ROS indirectly provoke DNA oxidation and mutations evidenced by the formation of 8 oxo-deoxyguanosine (8-oxo-dG) in guanine bases, and are involved in skin cancer development [ 34 , 35 ]. The direct implications of ROS in photoaging have been thoroughly investigated (for review, see [ 31 , 36 , 37 , 38 ]). Lipid oxidation products generated from PUFA oxidation by UV radiation largely contribute to the photoaging process, particularly aldehydic RCS (HNE, MDA, acrolein) [ 22 , 24 , 25 , 39 , 40 , 41 , 42 , 43 ].…”

“…As recently reviewed by Bernerd et al [ 37 ] and Papaccio et al [ 58 ], chronic UV exposure promotes protein oxidation and carbonylation in the epidermis and dermis, and the accumulation of oxidatively modified and damaged proteins. RCS-adducts are detected in human skin biopsies, in keratinocytes, fibroblasts [ 59 , 60 ] and ECM [ 61 ].…”