Acute Ultraviolet Radiation Exposure Research Articles

Seasonal Tanning-Induced Increases in Skin Pigmentation Do Not Affect Nitric Oxide-Mediated Vasodilation of the Cutaneous Microvasculature

Acute ultraviolet radiation (UVR) exposure reduces nitric oxide (NO)-dependent cutaneous vasodilation. Additionally, increased constitutive skin melanin concentrations are associated with reduced NO-dependent cutaneous vasodilation. However, the impact of seasonal tanning-induced increases in skin melanin concentration on NO-dependent cutaneous vasodilation has not been investigated. PURPOSE: To investigate the effect of seasonal tanning-induced increases in skin melanin on the NO-dependent cutaneous vasodilation response to local heating. We hypothesized that NO-dependent cutaneous vasodilation would be reduced in tanned skin relative to untanned skin. METHODS: Three intradermal microdialysis fibers were placed in the ventral upper arm (least sun exposed), ventral forearm (moderately sun exposed), and dorsal forearm (most sun exposed) of seven adults (33 ± 14 yrs; 4M/3F) with light-to-moderate constitutive skin pigmentation. Differences in sun exposure among the sites was confirmed using the melanin-index (M-index; an index of skin pigmentation), measured via skin reflectance spectrophotometry. Lactated Ringer’s solution was perfused through the microdialysis fibers while local heating to 42°C induced cutaneous vasodilation. After attaining a stable plateau in cutaneous blood flow, 15mM NG-nitro-L-arginine methyl ester (L-NAME; NO synthase inhibitor) was perfused at all sites to quantify NO-mediated vasodilation. Red cell flux was measured using laser-Doppler flowmetry (LDF). Cutaneous vascular conductance (CVC=LDF/mean arterial pressure) was calculated for each phase of the local heating response (i.e., baseline, initial peak, local heating plateau, post L-NAME plateau) and expressed as percent maximum (%CVCmax; 28mM sodium nitroprusside + 43°C local heating). RESULTS: M-index was highest (i.e., skin pigmentation was darkest) in the dorsal forearm (50.5 ± 11.8 a.u.) compared to the ventral forearm (37.5 ± 7.4 a.u.; p ≤ 0.03) and upper arm (30.2 ± 5.1 a.u.; p ≤ 0.001). There were no baseline (p ≥ 0.37), initial peak (p ≥ 0.22), post L-NAME plateau (p ≥ 0.12), or maximal CVC (p ≥ 0.23) differences among the three sites. Likewise, the magnitude of the local heating plateau was not different among the three sites (dorsal: 88±17%; ventral: 81±20%; upper: 90±12%; p ≥ 0.16), nor was NO-mediated vasodilation (dorsal: 59±15%; ventral: 54±13%; upper: 55±11.0%; p ≥ 0.79). CONCLUSION: These data suggest that, in contrast to the effects of acute UVR exposure or a constitutively dark skin pigmentation, seasonal tanning-induced increases in skin pigmentation do not alter NO-dependent cutaneous vasodilation responses to local heating. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Transcriptomic Effects of Acute Ultraviolet Radiation Exposure on Two Syntrichia Mosses.

Ultraviolet radiation (UVR) is a major environmental stressor for terrestrial plants. Here we investigated genetic responses to acute broadband UVR exposure in the highly desiccation-tolerant mosses Syntrichia caninervis and Syntrichia ruralis, using a comparative transcriptomics approach. We explored whether UVR protection is physiologically plastic and induced by UVR exposure, addressing the following questions: (1) What is the timeline of changes in the transcriptome with acute UVR exposure in these two species? (2) What genes are involved in the UVR response? and (3) How do the two species differ in their transcriptomic response to UVR? There were remarkable differences between the two species after 10 and 30 min of UVR exposure, including no overlap in significantly differentially abundant transcripts (DATs) after 10 min of UVR exposure and more than twice as many DATs for S. caninervis as there were for S. ruralis. Photosynthesis-related transcripts were involved in the response of S. ruralis to UVR, while membrane-related transcripts were indicated in the response of S. caninervis. In both species, transcripts involved in oxidative stress and those important for desiccation tolerance (such as late embryogenesis abundant genes and early light-inducible protein genes) were involved in response to UVR, suggesting possible roles in UVR tolerance and cross-talk with desiccation tolerance in these species. The results of this study suggest potential UVR-induced responses that may have roles outside of UVR tolerance, and that the response to URV is different in these two species, perhaps a reflection of adaptation to different environmental conditions.

Osmolyte transporter expression is reduced in photoaged human skin: Implications for skin hydration in aging.

Aging is characterized by the deterioration of tissue structure and function. In skin, environmental factors, for example, ultraviolet radiation (UVR), can accelerate the effects of aging such as decline in barrier function and subsequent loss of hydration. Water homeostasis is vital for all cellular functions and it is known that organic osmolyte transport is critical to this process. Therefore, we hypothesized that as we age, these tightly controlled physiological mechanisms become disrupted, possibly due to loss of transporter expression. We investigated this in vivo, using human skin samples from photoprotected and photoexposed sites of young and aged volunteers. We show a reduction in keratinocyte cell size with age and a downregulation of osmolyte transporters SMIT and TAUT with both chronic and acute UVR exposure. Single‐cell live imaging demonstrated that aged keratinocytes lack efficient cell volume recovery mechanisms possessed by young keratinocytes following physiological stress. However, addition of exogenous taurine significantly rescued cell volume; this was corroborated by a reduction in TAUT mRNA and protein in aged, as compared to young, keratinocytes. Collectively, these novel data demonstrate that human epidermal keratinocytes possess osmolyte‐mediated cell volume regulatory mechanisms, which may be compromised in aging. Therefore, this suggests that organic osmolytes—especially taurine—play a critical role in cutaneous age‐related xerosis and highlights a fundamental mechanism, vital to our understanding of the pathophysiology of skin aging.

Innate resistance of PSII efficiency to sunlight stress is not an advantage for cyanobacteria compared to eukaryotic phytoplankton

The effects of acute solar radiation stress on photosynthetic efficiency in freshwater unialgal cultures representing three phytoplankton pigment groups were measured by pulse amplitude modulated fluorometry (Walz Phyto-PAM) and compared to previous observations on field populations. Ultraviolet radiation (UVR) (UV-B and UV-A) induced a loss of photochemical quantum efficiency (Fv/Fm) in all 13 taxa examined in culture, while effects of photosynthetically active radiation (PAR) were smaller and often insignificant. Cyanobacteria were the most sensitive to PAR and UVR stress, chlorophytes the least and chromophytes intermediate but variable. The kinetics of maximal (Fm) and minimal (F0) fluorescence responses suggested uncoupling of antenna pigments from reaction centers (decreased Fm) persistent after dark adaptation was a common response, in particular for chromophytes, while the extent of impairment from damaged reaction centers (increased F0) was more variable. Changes in Fv/Fm with irradiance exposure were well described by the Kok model of photoinhibition and indicated that damage, rather than recovery, processes were predictive of acute cumulative inhibition. Field populations of cyanobacteria and chromophytes tended to greater tolerance and lower damage rates than laboratory strains. The results for cultures under standardized conditions supported field results in showing cyanobacteria more sensitive to acute UVR exposure than eukaryotic algae, and thus lacking any innate resistance of photosystem II to sunlight stress that might help explain their success in surface bloom formation.

The Modulating Effects of Sunscreen and Simulated Sweat on Ultraviolet Radiation‐ Induced Microvascular Dysfunction in the Human Cutaneous Vasculature

After acute ultraviolet radiation (UVR) exposure, nitric oxide (NO)‐mediated vasodilation is attenuated in the cutaneous microvasculature, likely via increased oxidative stress. Application of sunscreen to the skin protects from, while sweat on the skin may exacerbate, deleterious effects of UVR, including the erythema. However, it is unknown whether the presence of sunscreen or sweat on the skin influences the effect of UVR exposure on NO‐dependent vasodilation, a marker of skin vascular health.PurposeTo compare the impact of acute UVR, UVR with sunscreen (+SS), and UVR with simulated sweat (+SW) on NO‐mediated vasodilation in the cutaneous microcirculation. We hypothesized that +SS would blunt and +SW would augment the reduction in NO‐dependent vasodilation following acute UVR exposure.MethodsThree intradermal microdialysis fibers were placed in the ventral skin of the left forearm and a single fiber was placed in the right forearm of 13 healthy adults (24±1 yr; 6M/7F) with mild to moderate skin pigmentation (M‐index 30–46). Sites on the left forearm were randomly assigned to UVR exposure (450 mJ/cm2), UVR+SS (SPF‐50 chemical sunscreen), or UVR+SW (64 mmol Na+, 2.1 mmol K+), while the sight on the right forearm served as a non‐UVR exposed control (CON). Following UVR exposure, a standardized local heating (42°C) protocol induced cutaneous vasodilation. After attaining a plateau blood flow, 15mM NG‐nitro‐L‐arginine methyl ester (L‐NAME; NO synthase inhibitor) was infused at all sites to quantify the NO contribution to cutaneous vasodilation. Red cell flux was measured at each site (laser‐Doppler flowmetry) and cutaneous vascular conductance (CVC=flux/MAP) was expressed as a percentage of maximum (%CVCmax; 28mM sodium nitroprusside+43°C) for each phase of the local heating response. The NO‐mediated contribution (%NO) was calculated as the difference between the local heating and L‐NAME plateaus.ResultsThere were no differences in %CVCmax between treatments at baseline (p≥0.55), initial peak (p≥0.40), or heating plateau (p≥0.44). However, UVR blunted %NO compared to CON (CON: 40.8±4.8 vs UVR: 28.0±6.7%; p<0.01). The attenuation in %NO was prevented by sunscreen (UVR: 28.0±6.7 vs UVR+SS: 54.5±5.8%; p<0.01) and by simulated sweat (UVR: 28.0±6.7 vs UVR+SW: 45.8±5.2%; p<0.01). Further, when sunscreen was applied prior to UVR, UVR exposure actually augmented %NO compared to CON (UVR+SS: 54.5±5.8% vs CON: 40.8±4.8; p<0.01) or when sweat was on the skin (UVR+SS: 54.5±5.8 vs UVR+SW: 45.8±5.2%; p<0.01).ConclusionAcute broad spectrum UVR exposure attenuates NO‐mediated vasodilation in the cutaneous microvasculature. The presence of sunscreen or sweat on the skin may play a protective role against this effect, and UVR may actually augment NO‐mediated vasodilation in the presence of a chemical sunscreen.Support or Funding InformationACSM Foundation Doctoral Student Research Grant #17‐00552 and NIH T‐32 Grant #5T32AG049676‐03This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Differential reorganisation of cutaneous elastic fibres: a comparison of the in vivo effects of broadband ultraviolet B versus solar simulated radiation

Long-term exposure of human skin to ultraviolet radiation (UVR) in sunlight negatively impacts its appearance and function with photoaged skin having a characteristic leathery, rough appearance, with deep wrinkles. These clinical features of photodamage are thought to result from UVR-induced remodelling of the dermal extracellular matrix, particularly the elastic fibre system. There are few in vivo human data on the impact of acute UVR exposure on this fibre system and particularly solar-simulated radiation (SSR)-mediated effects. We examined the differential effect of broadband UVB and SSR on the human dermal elastic fibre system, and specifically the microfibrillar components fibrillin-1, fibulin-2 and fibulin-5. Healthy white Caucasian adults (skin type II–III) were recruited and irradiated with 3× their minimal erythema dose of broadband UVB (n = 6) or SSR (n = 6) on photoprotected buttock skin. Punch biopsies were taken 24 h after irradiation and from unirradiated control skin. Overall, histological assessment of elastic fibres revealed significantly less elastic fibre staining in broadband UVB (P = 0.004) or SSR (P = 0.04) irradiated skin compared to unirradiated control skin. Significantly less staining of fibrillin-1-positive microfibrils was also observed in the papillary dermis of UVB irradiated skin (P = 0.02) but not skin exposed to SSR. Conversely, immunohistochemistry for fibulin-5-positive microfibrils revealed significantly less expression in skin exposed to SSR (P = 0.04) but not to broadband UVB. There was no significant change in fibulin-2-positive microfibrils following either broadband UVB or SSR irradiation. Thus, broadband UVB and SSR mediate differential effects on individual components of the dermal elastic fibre network in human skin. Further human studies are required to explore the mechanisms underlying these findings and the impact of potential photoprotective agents.

Attenuation of UVR-induced vitamin D3 synthesis in a mouse model deleted for keratinocyte lathosterol 5-desaturase

The lower risk of some internal cancers at lower latitudes has been linked to greater sun exposure and consequent higher levels of ultraviolet radiation (UVR)-produced vitamin D3 (D3). To separate the experimental effects of sunlight and of all forms of D3, a mouse in which UVR does not produce D3 would be useful.To this end we have generated mice carrying a modified allele of sterol C5-desaturase (Sc5d), the gene encoding the enzyme that converts lathosterol to 7-dehydrocholesterol (7-DHC), such that Sc5d expression can be inactivated using the Cre/lox site-specific recombination system. By crossing to mice with tissue-specific expression of Cre or CreER2 (Cre/estrogen receptor), we generated two lines of transgenic mice. One line has constitutive keratinocyte-specific inactivation of Sc5d (Sc5dk14KO). The other line (Sc5dk14KOi) has tamoxifen-inducible keratinocyte-specific inactivation of Sc5d.Mice deleted for keratinocyte Sc5d lose the ability to increase circulating D3 following UVR exposure of the skin. Thus, unlike in control mice, acute UVR exposure did not affect circulating D3 level in inducible Sc5dk14KOi mice.Keratinocyte-specific inactivation of Sc5d was proven by sterol measurement in hair – in control animals lathosterol and cholesta-7,24-dien-3β-ol, the target molecules of SC5D in the sterol biosynthetic pathways, together constituted a mean of 10% of total sterols; in the conditional knockout mice these sterols constituted a mean of 56% of total sterols. The constitutive knockout mice had an even greater increase, with lathosterol and cholesta-7,24-dien-3β-ol accounting for 80% of total sterols.In conclusion, the dominant presence of the 7-DHC precursors in hair of conditional animals and the lack of increased circulating D3 following exposure to UVR reflect attenuated production of the D3 photochemical precursor 7-DHC and, consequently, of D3 itself. These animals provide a useful new tool for investigating the role of D3 in UVR-induced physiological effects and, more broadly, for investigations of the cholesterol synthetic pathway in the skin and other targeted tissues.

Solar ultraviolet radiation exposure influences the immune response to immunization: Results from an Australian clinical trial

Background Exposure to ultraviolet radiation (UVR) causes systemic immune suppression. The effect of natural levels of UVR exposure on the primary immune response to vaccination has not been previously reported. Method The Australian Ultraviolet Radiation and Immunity Study was conducted in the Australian cities of Canberra (35o2’S) and Townsville (19o1’S) from July 1010 to August 2011. Healthy volunteers (n=222) aged 18–40 years were immunised subcutaneously with keyhole limpet haemocyanin (KLH). Acute personal UVR exposure was measured by electronic UVR wrist dosimeters worn for five days pre- and post-vaccination, and by sun exposure diary. Cumulative UVR exposure was quantified by microtopographic analysis of silicone impressions of sun-exposed skin. Potential confounders were measured (e.g. serum 25-OH vitamin D). Immune function measured over a 21-day period post-vaccination included: anti-KLH IgG1 levels; KLH-specific delayed-type hypersensitivity (DTH) response; and quantification of T-helper (CD4+) lymphocyte subsets. Results In multiple regression models, higher acute UVR exposure on the day prior (‘Day 5’) to vaccination (p=0.015), and Days 5-8 and 5-9 (p=0.039 and p=0.025, respectively) were associated with reduced DTH response to KLH challenge at day 21 post-vaccination.”Change in T-helper 17 cell percentage between pre- and post-vaccination time points differed in direction when comparing the low and high UVR exposure groups (-0.39%vs.0.31%; p=0.004). There was no association between UVR exposure and anti-KLH IgG1. 25-OH vitamin D was not associated with immune function outcomes. Conclusions Acute UVR exposures, relevant to day-to-day activities, modulates the cell-mediated primary immune responses to KLH vaccination.

Ultraviolet Keratitis Among Mountaineers and Outdoor Recreationalists

Ultraviolet (UV) keratitis is a self-limited, inflammatory condition resulting in pain and temporary visual disturbance following acute UV radiation exposure. It may afflict mountaineers and other outdoor recreationalists because snow, water, and sand reflect a high percentage of UV radiation reaching the earth's surface. We examined the cases of UV keratitis that have occurred on National Outdoor Leadership School (NOLS) courses in order to better understand its epidemiology and to help prevent this affliction on wilderness expeditions. We retrospectively reviewed all cases of UV keratitis that occurred on NOLS courses from 1984-2009. Subject demographics and contributing factors were recorded and descriptive information reported. Fifteen cases of UV keratitis occurred during the study period with an overall incidence of 0.06% in those exposed. All cases occurred in mountainous or snowy terrain except one case which occurred while boating on a river. Thirteen of the 15 (87%) cases occurred in participants who were not wearing sunglasses. Two cases (13%) occurred in participants who were wearing sunglasses without side shields. Ten cases (71%) occurred in sunny conditions, and 4 cases (29%) occurred in cloudy or low visibility conditions. In all cases, symptoms resolved within 36 hours after cessation of UV exposure. Appropriate eye protection, including adequate lenses with appropriate side shields, should be worn in mountain or water environments in order to prevent UV keratitis. This data supports the conventional conception of UV keratitis as a relatively mild and self-limited condition, if treated appropriately.

Ultraviolet Radiation-Induced Corneal Degeneration in 129 Mice

Ultraviolet radiation (UVR) is a risk factor for the development of ocular disease in humans, including acute photokeratitis, chronic corneal spheroidal degeneration, and cataract formation. This report describes the ocular lesions seen in 21 mice chronically exposed to UVR as part of a skin carcinogenicity study. All globes were affected to varying degrees. The primary lesion, not previously reported in UVR-exposed mice, was marked loss of keratocytes relative to age-matched controls. Secondary lesions included corneal stromal thinning, keratoconus, corneal vascularization and fibrosis, keratitis, globe rupture, and phthisis bulbi. In addition, more than 90% of UVR-exposed and unexposed lenses had evidence of cataract formation; this is the first report of the occurrence of spontaneous cataracts in 129 mice. In a subsequent study, apoptotic cells were identified histologically and by cleaved caspase 3 immunoreactivity in the corneal epithelium and, less commonly, in the corneal stroma after acute UVR exposure. Based on this finding, we propose that the loss of keratocytes observed in the chronic study was due to UVR-induced apoptosis.