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In a placebo-controlled trial involving immunosuppressed organ-transplant recipients, oral nicotinamide (500 mg twice daily) for 12 months did not lead to lower numbers of keratinocyte cancers or actinic keratoses.

Matrix metalloproteinases (MMPs) are zinc-containing endopeptidases with an extensive range of substrate specificities. Collectively, these enzymes are able to degrade various components of extracellular matrix (ECM) proteins. Based on their structure and substrate specificity, they can be categorized into five main subgroups, namely (1) collagenases (MMP-1, MMP-8 and MMP-13); (2) gelatinases (MMP-2 and MMP-9); (3) stromelysins (MMP-3, MMP-10 and MMP-11); (4) matrilysins (MMP-7 and MMP-26); and (5) membrane-type (MT) MMPs (MMP-14, MMP-15, and MMP-16). The alterations made to the ECM by MMPs might contribute in skin wrinkling, a characteristic of premature skin aging. In photocarcinogenesis, degradation of ECM is the initial step towards tumor cell invasion, to invade both the basement membrane and the surrounding stroma that mainly comprises fibrillar collagens. Additionally, MMPs are involved in angiogenesis, which promotes cancer cell growth and migration. In this review, we focus on the present knowledge about premature skin aging and skin cancers such as basal cell carcinoma (BCC), squamous cell carcinoma (SCC), and melanoma, with our main focus on members of the MMP family and their functions.

Cutaneous melanoma causes 55 500 deaths annually. The incidence and mortality rates of the disease differ widely across the globe depending on access to early detection and primary care. Once melanoma has spread, this type of cancer rapidly becomes life-threatening. For more than 40 years, few treatment options were available, and clinical trials during that time were all unsuccessful. Over the past 10 years, increased biological understanding and access to innovative therapeutic substances have transformed advanced melanoma into a new oncological model for treating solid cancers. Treatments that target B-Raf proto-oncogene serine/threonine-kinase (BRAF)V600 (Val600) mutations using selected BRAF inhibitors combined with mitogen-activated protein kinase inhibitors have significantly improved response and overall survival. Furthermore, advanced cutaneous melanoma has developed into a prototype for testing checkpoint-modulating agents, which has increased hope for long-term tumour containment and a potential cure. These expectations have been sustained by clinical success with targeted agents and antibodies that block programmed cell-death protein 1 in locoregional disease, which induces prolongation of relapse-free, distant-metastasis-free, and overall survival times.

l-Ascorbic acid (LAA) is considered a powerful antioxidant that protects skin from premature aging. Maintaining the stability of vitamin C remains the biggest challenge in cosmeceuticals. Our main aim is the entrapment of high dose of vitamin C in spanlastic vesicles to provide maximum stability and efficacy. LAA-loaded spanlastics were prepared by ethanol injection method and were characterized for entrapment efficiency (EE%), particles size (PS), polydispersity index (PDI), zeta potential, deformability index (DI) and in vivo skin permeation. Selected spanlastics formula composed of span 60 and tween 60 (5:1) showed highest EE% of 89.77 ± 3.61% (w/w), high deformability of 11.13 ± 1.145 as well as good physical and chemical stability for 6 months. Improved drug penetration into stratum corneum (SC) was obtained from spanlastics compared to topical LAA solution. Quantitative real time PCR revealed that MMP2 and MMP9 levels were significantly suppressed in response to LAA spanlastics treated rats by 30.4% and 65.3%, respectively, when compared to the control group after exposure to UV irradiation. Results were confirmed by western blot analysis. Histopathological study of rat skin after UV irradiation revealed that application of LAA-loaded spanlastics provided the highest skin protection compared to UVB and LAA solution treated group which was evident by the normal thick epidermal morphology and the densely arranged dermal collagen fibers. LAA-loaded spanlastics successfully improved LAA stability, skin permeation and antioxidant protection against skin photodamage.

In vitro and animal studies have demonstrated that topical application and oral consumption of pomegranate reduces UVB-induced skin damage. We therefore investigated if oral pomegranate consumption will reduce photodamage from UVB irradiation and alter the composition of the skin microbiota in a randomized controlled, parallel, three-arm, open label study. Seventy-four female participants (30–45 years) with Fitzpatrick skin type II-IV were randomly assigned (1:1:1) to 1000 mg of pomegranate extract (PomX), 8 oz of pomegranate juice (PomJ) or placebo for 12 weeks. Minimal erythema dose (MED) and melanin index were determined using a cutometer (mexameter probe). Skin microbiota was determined using 16S rRNA sequencing. The MED was significantly increased in the PomX and PomJ group compared to placebo. There was no significant difference on phylum, but on family and genus level bacterial composition of skin samples collected at baseline and after 12 week intervention showed significant differences between PomJ, PomX and placebo. Members of the Methylobacteriaceae family contain pigments absorbing UV irradiation and might contribute to UVB skin protection. However, we were not able to establish a direct correlation between increased MED and bacterial abundance. In summary daily oral pomegranate consumption may lead to enhanced protection from UV photodamage.

Melanoma survivors are at increased risk of developing a second primary melanoma; however, some report sub-optimal sun behaviors and sunburns. We tested the effectiveness of a wearable device with ultraviolet radiation (UVR)-sensing technology to improve sun behaviors and reduce sunburns in cutaneous melanoma survivors. We conducted a randomized controlled trial using Shade 2, a commercially available wrist device that measures UVR. The intervention group received the device and mobile application notifications about their exposure and prompts to use sunscreen. The control group received the device and a separate research mobile application without information about their exposure or notifications. Participants wore the device for 12 weeks and self-reported sun behaviors before, during, and after the intervention. The primary outcome was a composite score of sun protection behaviors at week 12. 386 participants were randomized (186 control, 182 intervention). Most were female and 5+ years past their first melanoma diagnosis. The average age was 56 years. Most (93%) completed the study, though 40% experienced device issues. No meaningful differences were observed in self-reported sun protection behaviors at week 12 (controls 3.0±0.5 vs. intervention 2.9±0.5, p = 0.06), any sunburn during the intervention period (controls 14.4% vs. intervention 12.7%, p = 0.75), or average daily objective UVR exposure (controls median 87 vs. intervention 83 J/m2, p = 0.43). Wearing a device that measured and alerted melanoma survivors to UVR exposure did not result in different sun behaviors, exposure, or sunburns relative to controls. The technology needs refinement before further attempts to assess the effectiveness of self-monitoring UVR exposure. NCT03927742.

Access to DNA packaged in nucleosomes is critical for gene regulation, DNA replication and DNA repair. In humans, the UV-damaged DNA-binding protein (UV-DDB) complex detects UV-light-induced pyrimidine dimers throughout the genome; however, it remains unknown how these lesions are recognized in chromatin, in which nucleosomes restrict access to DNA. Here we report cryo-electron microscopy structures of UV-DDB bound to nucleosomes bearing a 6–4 pyrimidine–pyrimidone dimer or a DNA-damage mimic in various positions. We find that UV-DDB binds UV-damaged nucleosomes at lesions located in the solvent-facing minor groove without affecting the overall nucleosome architecture. In the case of buried lesions that face the histone core, UV-DDB changes the predominant translational register of the nucleosome and selectively binds the lesion in an accessible, exposed position. Our findings explain how UV-DDB detects occluded lesions in strongly positioned nucleosomes, and identify slide-assisted site exposure as a mechanism by which high-affinity DNA-binding proteins can access otherwise occluded sites in nucleosomal DNA. Cryo-electron microscopy structures reveal that the DNA-repair factor UV-DDB exposes inaccessible nucleosome lesions for binding by inducing a translational shift in the nucleosome position.

The oral administration of antioxidants may suppress UV-B-induced skin damage. HITHION YH-15, the extract of Torula yeast ( Cyberlindnera jadinii ), is rich in cysteine-containing peptides such as reduced and oxidized glutathione (GSH and GSSG), γ-glutamylcysteine (γ-Glu-Cys), and cysteinylglycine (Cys-Gly). These four constituents are termed cysteine peptides. In this study, we investigated the protective effects of cysteine peptides against UV-B in a randomized, placebo-controlled, double-blind, parallel-group study. A total of 90 healthy males and females aged 30–59 years were enrolled and randomized into two groups of 45 individuals each (cysteine peptides (48 mg/day) and placebo). Changes in UV-B-induced erythema and pigmentation were compared between groups after 5 weeks of test food intake. The minimal erythema dose (MED) significantly increased (* p  = 0.019) in the cysteine peptides group compared to that in the placebo group, indicating suppression of UV-B-induced erythema. ΔL* value significantly increased (*** p  < 0.0001) in the cysteine peptides group compared to that in the placebo, indicating pigmentation suppression. We demonstrated that oral administration of cysteine peptides suppresses UV-B-induced erythema and pigmentation through multiple mechanisms. Thus, cysteine peptides may find use as nutricosmetics for maintaining skin health and well-being. UMIN Clinical Trials Registry ID: UMIN 000050157.

Background Skin cancers resulting from excessive exposure to solar ultraviolet (UV) radiation are on the rise. This study aims to investigate the impact of facial-aging app intervention on promoting safe and healthy behaviors and its influence on reducing students' UV exposure. Method Utilizing a Pretest–Posttest repeated-measures design, we developed a theory-guided web app on the WhatsApp platform, named the Sunshine and Skin Health app. This app allows users to visualize their altered faces in three stages of adolescence, middle age, and old age based on sun protection behavior. The intervention continued within WhatsApp, incorporating 27 health messages grounded in the PMT theory, eight educational files, and a skin cancer video clip. The primary outcome is the change in sun protection behavior between the two groups (intervention and control) immediately after the intervention (T2) and the secondary outcome is the change in sun protection behavior between the two groups at 3 months follow-up (T3). The data are analyzed in SPSS 22 and a significance level of 0.05 is considered. Results The results revealed no significant difference between the two groups before the intervention. However, in the intervention group, there were significant differences in the utilization of sunglasses, hats, and sunscreen in the last month, as well as sunscreen reapplication after washing their hands and face, both immediately after the intervention and at the 3-month follow-up, compared to the control group ( P  = 0.001). Furthermore, a significant intervention effect, time effect, and interaction effect between group and time were observed in behaviors related to using sunscreen in the last month and sunscreen reapplication after washing hands and face ( P  = 0.001). Specifically, the intervention group exhibited a significant difference from Time 1 to 2 and from Time 1 to 3 ( p  = 0.001), but no significant difference from Time 2 to 3. In contrast, the control group did not show any significant differences over time. Conclusions This study indicated that the Facial-Aging web app can effectively encourage safe behaviors in sunlight. To ensure the maintenance and sustainability of these behaviors over the long term, it is crucial to consider implementing booster sessions. Trial registration Iranian Registry of Clinical Trials IRCT20200924048825N1. Registered prospectively on 8 February 2021.

The production of melanin pigments by melanocytes and their quantity, quality, and distribution play a decisive role in determining human skin, eye, and hair color, and protect the skin from adverse effects of ultraviolet radiation (UVR) and oxidative stress from various environmental pollutants. Melanocytes reside in the basal layer of the interfollicular epidermis and are compensated by melanocyte stem cells in the follicular bulge area. Various stimuli such as eczema, microbial infection, ultraviolet light exposure, mechanical injury, and aging provoke skin inflammation. These acute or chronic inflammatory responses cause inflammatory cytokine production from epidermal keratinocytes as well as dermal fibroblasts and other cells, which in turn stimulate melanocytes, often resulting in skin pigmentation. It is confirmed by some recent studies that several interleukins (ILs) and other inflammatory mediators modulate the proliferation and differentiation of human epidermal melanocytes and also promote or inhibit expression of melanogenesis-related gene expression directly or indirectly, thereby participating in regulation of skin pigmentation. Understanding of mechanisms of skin pigmentation due to inflammation helps to elucidate the relationship between inflammation and skin pigmentation regulation and can guide development of new therapeutic pathways for treating pigmented dermatosis. This review covers the mechanistic aspects of skin pigmentation caused by inflammation.