Cybermedlife - Therapeutic Actions Sunlight Exposure - UVB Light

Ultraviolet B Exposure Inhibits Angiotensin II-Induced Abdominal Aortic Aneurysm Formation in Mice by Expanding CD4Foxp3Regulatory T Cells. 📎

Abstract Title: Ultraviolet B Exposure Inhibits Angiotensin II-Induced Abdominal Aortic Aneurysm Formation in Mice by Expanding CD4Foxp3Regulatory T Cells. Abstract Source: J Am Heart Assoc. 2017 Aug 31 ;6(9). Epub 2017 Aug 31. PMID: 28860231 Abstract Author(s): Tomohiro Hayashi, Naoto Sasaki, Tomoya Yamashita, Taiji Mizoguchi, Takuo Emoto, Hilman Zulkifli Amin, Keiko Yodoi, Takuya Matsumoto, Kazuyuki Kasahara, Naofumi Yoshida, Tokiko Tabata, Naoki Kitano, Atsushi Fukunaga, Chikako Nishigori, Yoshiyuki Rikitake, Ken-Ichi Hirata Article Affiliation: Tomohiro Hayashi Abstract: BACKGROUND: Pathogenic immune responses are known to play an important role in abdominal aortic aneurysm (AAA) development. Ultraviolet B (UVB) irradiation has been demonstrated to have therapeutic potential not only for cutaneous diseases but also for systemic inflammatory diseases in mice by suppressing immunoinflammatory responses. We investigated the effect of UVB irradiation on experimental AAA. METHODS AND RESULTS: We used an angiotensin II-induced AAA model in apolipoprotein E-deficient mice fed a high-cholesterol diet. Mice aged 10 weeks were irradiated with 5 kJ/mUVB once weekly for 6 weeks (UVB-irradiated, n=38; nonirradiated, n=42) and were euthanized for evaluation of AAA formation at 16 weeks. Overall, 93% of angiotensin II-infused mice developed AAA, with 60% mortality possibly because of aneurysm rupture. UVB irradiation significantly decreased the incidence (66%) and mortality (29%) of AAA (=0.004 and=0.006, respectively). UVB-irradiated mice had significantly smaller diameter AAA (=0.008) and fewer inflammatory cells in the aortic aneurysm tissue than nonirradiated mice, along with systemic expansion of CD4Foxp3regulatory T cells and decreased effector CD4CD44CD62LT cells in para-aortic lymph nodes. Genetic depletion of regulatory T cells abrogated these beneficial effects of UVB treatment, demonstrating a critical role of regulatory T cells. CONCLUSIONS: Our data suggest that UVB-dependent expansion of regulatory T cells has beneficial effects on experimental AAA and may provide a novel strategy for the treatment of AAA. Article Published Date : Aug 30, 2017

Demethoxycurcumin in combination with ultraviolet radiation B induces apoptosis through the mitochondrial pathway and caspase activation in A431 and HaCaT cells. 📎

Abstract Title: Demethoxycurcumin in combination with ultraviolet radiation B induces apoptosis through the mitochondrial pathway and caspase activation in A431 and HaCaT cells. Abstract Source: Tumour Biol. 2017 Jun ;39(6):1010428317706216. PMID: 28618944 Abstract Author(s): Yong Xin, Qian Huang, Pei Zhang, Wen Wen Guo, Long Zhen Zhang, Guan Jiang Article Affiliation: Yong Xin Abstract: Photodynamic therapy is widely used in the clinical treatment of tumors, especially skin cancers. It has been reported that the photosensitizer curcumin, in combination with ultraviolet radiation B, induces HaCaT cell apoptosis, and this effect may be due to the activation of caspase pathways. In this study, we examined the photodynamic effects of demethoxycurcumin, a more stable analogue of curcumin, to determine whether it could induce apoptosis in skin cancer cells. We investigated the effects of a combination of ultraviolet radiation B and demethoxycurcumin on apoptotic cell death in A431 and HaCaT cells and determined the molecular mechanism of action. Our results showed increased apoptosis with a combination of ultraviolet radiation B with demethoxycurcumin, as compared to ultraviolet radiation B or demethoxycurcumin alone. The combination of ultraviolet radiation B irradiation with demethoxycurcumin synergistically induced apoptotic cell death in A431 and HaCaT cells through activation of p53 and caspase pathways, as well as through upregulation of Bax and p-p65 expression and downregulation of Bcl-2, Mcl-1, and nuclear factor-κB expression. In addition, we found that reactive oxygen species significantly increased with treatment, and mitochondrial membrane potential depolarization was remarkably enhanced. In conclusion, our data indicate that demethoxycurcumin may be a promising photosensitizer for use in photodynamic therapy to induce apoptosis in skin cancer cells. Article Published Date : May 31, 2017

Enhancement of Vitamin D Metabolites in the Eye Following Vitamin D3 Supplementation and UV-B Irradiation. 📎

Abstract Title: Enhancement of Vitamin D Metabolites in the Eye Following Vitamin D3 Supplementation and UV-B Irradiation. Abstract Source: Curr Eye Res. 2012 May 25. Epub 2012 May 25. PMID: 22632164 Abstract Author(s): Yanping Lin, John L Ubels, Mark P Schotanus, Zhaohong Yin, Victorina Pintea, Bruce D Hammock, Mitchell A Watsky Article Affiliation: Department of Entomology&Cancer Center, University of California , Davis, CA , USA. Abstract: Purpose: This study was designed to measure vitamin D metabolites in the aqueous and vitreous humor and in tear fluid, and to determine if dietary vitamin D3 supplementation affects these levels. We also determined if the corneal epithelium can synthesize vitamin D following UV-B exposure. Methods: Rabbits were fed a control or vitamin D3 supplemented diet. Pilocarpine-stimulated tear fluid was collected and aqueous and vitreous humor were drawn from enucleated eyes. Plasma vitamin D was also measured. To test for epithelial vitamin D synthesis, a human corneal limbal epithelial cell line was irradiated with two doses of UV-B (10 and 20 mJ/cm(2)/day for 3 days) and vitamin D was measured in control or 7-dehydrocholesterol treated culture medium. Measurements were made using mass spectroscopy. Results: 25(OH)-vitamin D3 and 24,25(OH)(2)-vitamin D3 increased significantly following D3 supplementation in all samples except vitreous humor. Tear fluid and aqueous humor had small but detectable 1,25(OH)(2)-vitamin D3 levels. Vitamin D2 metabolites were observed in all samples. Vitamin D3 levels were below the detection limit for all samples. Minimal vitamin D3 metabolites were observed in control and UV-B-irradiated epithelial culture medium except following 7-dehydrocholesterol treatment, which resulted in a UV-B-dose dependent increase in vitamin D3, 25(OH)-vitamin D3 and 24,25(OH)(2)-vitamin D3. Conclusions: There are measurable concentrations of vitamin D metabolites in tear fluid and aqueous and vitreous humor, and oral vitamin D supplementation affects vitamin D metabolite concentrations in the anterior segment of the eye. In addition, the UV exposure results lead us to conclude that corneal epithelial cells are likely capable of synthesizing vitamin D3 metabolites in the presence of 7-dehydrocholesterol following UV-B exposure. Article Published Date : May 25, 2012

Effects of prior light exposure on early evening performance, subjective sleepiness, and hormonal secretion.

Abstract Title: Effects of prior light exposure on early evening performance, subjective sleepiness, and hormonal secretion. Abstract Source: Behav Neurosci. 2012 Feb ;126(1):196-203. Epub 2011 Dec 26. PMID: 22201280 Abstract Author(s): Mirjam Münch, Friedrich Linhart, Apiparn Borisuit, Susanne M Jaeggi, Jean-Louis Scartezzini Article Affiliation: Solar Energy and Building Physics Laboratory, Swiss Federal Institute of Technology, Lausanne. Abstract: In sighted humans, light intensity, timing, exposure duration, and spectral composition of light are important to entrain the endogenous circadian pacemaker to the 24-h day-night cycle. We tested the impact of two realistic office lighting conditions during the afternoon on subjective sleepiness, hormonal secretion, and cognitive performance in the early evening hours. Twenty-nine young subjects came twice and spent 8 h (12:00-20:00) in our laboratory, where they were exposed for 6 h to either artificial light (AL) or to mainly daylight (DL). In the early evening, we assessed their salivary cortisol and melatonin secretion, subjective sleepiness, and cognitive performance (n-back test) under dim light conditions. Subjects felt significantly more alert at the beginning of the evening after the DL condition, and they became sleepier at the end of the evening after the AL condition. For cognitive performance we found a significant interaction between light conditions, mental load (2- or 3-back task) and the order of light administration. On their first evening, subjects performed with similar accuracy after both light conditions, but on their second evening, subjects performed significantly more accurately after the DL in both n-back versions and committed fewer false alarms in the 2-back task compared to the AL group. Lower sleepiness in the evening was significantly correlated with better cognitive performance (p<.05). In summary, even short-term lighting conditions during the afternoon had an impact on cognitive task performance in the evening. This rapid effect was only distinguishable on the second day of training, when a difficult task had been sufficiently practiced. Article Published Date : Feb 01, 2012

The deceptive nature of UVA tanning versus the modest protective effects of UVB tanning on human skin. 📎

Abstract Title: The deceptive nature of UVA tanning versus the modest protective effects of UVB tanning on human skin. Abstract Source: Pigment Cell Melanoma Res. 2011 Feb ;24(1):136-47. Epub 2010 Oct 6. PMID: 20979596 Abstract Author(s): Yoshinori Miyamura, Sergio G Coelho, Kathrin Schlenz, Jan Batzer, Christoph Smuda, Wonseon Choi, Michaela Brenner, Thierry Passeron, Guofeng Zhang, Ludger Kolbe, Rainer Wolber, Vincent J Hearing Article Affiliation: Laboratory of Cell Biology, National Cancer Institute, Bethesda, MD, USA. Abstract: The relationship between human skin pigmentation and protection from ultraviolet (UV) radiation is an important element underlying differences in skin carcinogenesis rates. The association between UV damage and the risk of skin cancer is clear, yet a strategic balance in exposure to UV needs to be met. Dark skin is protected from UV-induced DNA damage significantly more than light skin owing to the constitutively higher pigmentation, but an as yet unresolved and important question is what photoprotective benefit, if any, is afforded by facultative pigmentation (i.e. a tan induced by UV exposure). To address that and to compare the effects of various wavelengths of UV, we repetitively exposed human skin to suberythemal doses of UVA and/or UVB over 2 weeks after which a challenge dose of UVA and UVB was given. Although visual skin pigmentation (tanning) elicited by different UV exposure protocols was similar, the melanin content and UV-protective effects against DNA damage in UVB-tanned skin (but not in UVA-tanned skin) were significantly higher. UVA-induced tans seem to result from the photooxidation of existing melanin and its precursors with some redistribution of pigment granules, while UVB stimulates melanocytes to up-regulate melanin synthesis and increases pigmentation coverage, effects that are synergistically stimulated in UVA and UVB-exposed skin. Thus, UVA tanning contributes essentially no photoprotection, although all types of UV-induced tanning result in DNA and cellular damage, which can eventually lead to photocarcinogenesis. Article Published Date : Feb 01, 2011
Therapeutic Actions Sunlight Exposure - UVB Light

NCBI pubmed

Signaling Mechanisms Regulating Diverse Plant Cell Responses to UVB Radiation.

Related Articles Signaling Mechanisms Regulating Diverse Plant Cell Responses to UVB Radiation. Biochemistry (Mosc). 2018 Jul;83(7):787-794 Authors: Fraikin GY Abstract UVB radiation (290-320 nm) causes diverse effects in plant cells that vary with the fluence rate of exposure. High fluence rates of UVB radiation cause damage to DNA and formation of reactive oxygen species in mitochondria and chloroplasts, which lead to oxidation of membrane proteins and lipids and inhibition of cellular functions. In response to oxidative stress, mitochondrial transmembrane potential dissipates, resulting in cytochrome c release and activation of metacaspases. This leads to the apoptosis-like cell death. The signaling mechanism based on UVB DNA damage includes checkpoint activation, cell-cycle arrest, and finally programmed cell death with characteristic DNA fragmentation and morphological hallmarks typical of apoptotic cells. Recently, it was shown that among the components of this signaling mechanism the transcriptional factor SOG1 (suppressor of gamma response 1) plays a key role in regulation of programmed cell death in plants. In contrast to its damaging effects, UVB radiation at low fluence rates can act as a regulatory signal that is specifically perceived by plants to promote acclimation and survival in sunlight. The protective action of UVB is based on expression of various genes, including those encoding flavonoid synthesis enzymes that provide a UVB-absorbing sunscreen in epidermal tissues and DNA photorepair enzymes. These processes are mediated by the UVB photoreceptor UVR8, which has been recently characterized at the molecular level. Now progress is made in uncovering the UVR8-mediated signaling pathway mechanism in the context of UVB photon perception and revealing the biochemical components of the early stages of light signal transduction. In this review, attention is focused on the achievements in studying these UVB-induced signaling processes. PMID: 30200863 [PubMed - in process]

Hydrogen ameliorates oxidative stress via PI3K-Akt signaling pathway in UVB-induced HaCaT cells.

Related Articles Hydrogen ameliorates oxidative stress via PI3K-Akt signaling pathway in UVB-induced HaCaT cells. Int J Mol Med. 2018 Jun;41(6):3653-3661 Authors: Zhang B, Zhao Z, Meng X, Chen H, Fu G, Xie K Abstract Chronic ultraviolet (UV) exposure-induced oxidative stress is associated with the pathogenesis of skin damage. However, the nuclear factor erythroid‑2‑related factor 2 (Nrf2) pathway is a critical factor in protecting cells against UVB‑induced injury through inhibiting oxidative stress. Furthermore, Nrf2 activation requires the involvement of the phosphoinositide-3 kinase (PI3K)/protein kinase B (AKT) pathway, which has a major role in survival of various cell types. Molecular hydrogen exerts protective effects on UV‑induced injury, but the underlying mechanisms have remained elusive. The present study assessed the protective effects of hydrogen against oxidative stress‑induced injury caused by UVB irradiation and investigated the molecular mechanisms. In vitro, UVB‑induced HaCaT cells were collected for the detection of reactive oxygen species, 8‑iso‑prostaglandin F2α, malondialdehyde via fluorescence spectrometry and ELISA; cell activity and cytotoxicity by MTT and lactate dehydrogenase assays, respectively. Additionally, the expression level of PI3K, Akt, Nrf2 and heme oxygenase‑1 (HO‑1) were investigated using western blot, etc. All of the results indicated that hydrogen decreased the levels of reactive oxygen species, 8‑iso‑prostaglandin F2α and malondialdehyde, and promoted the UVB exposure‑induced expression of PI3K, Akt, Nrf2 and heme oxygenase‑1 in HaCaT cells. Of note, PI3K inhibition partially reversed the effects of hydrogen on UVB‑induced HaCaT cells. Therefore, hydrogen effectively protects cells from UVB radiation‑induced oxidative stress by inhibiting Nrf2/HO‑1 activation through the PI3K/Akt signaling pathway. PMID: 29532858 [PubMed - indexed for MEDLINE]

The use of satellite data to measure ultraviolet-B penetrance and its potential association with age of multiple sclerosis onset.

Related Articles The use of satellite data to measure ultraviolet-B penetrance and its potential association with age of multiple sclerosis onset. Mult Scler Relat Disord. 2018 Apr;21:30-34 Authors: Amram O, Schuurman N, Randall E, Zhu F, Saeedi J, Rieckmann P, Yee I, Tremlett H Abstract BACKGROUND: Studies have indicated an association between low Ultraviolet B (UVB) exposure and an increased risk of developing multiple sclerosis (MS). Few studies, however, have explored whether UVB exposure is associated with the age at MS symptom onset. OBJECTIVE: We investigated the potential association between cumulative early life ambient UVB exposure and age at MS onset, using satellite data to measure ambient UVB exposure. METHODS: Adult onset MS patients were selected from the University of British Columbia's MS genetic database (1980-2005). Patients' places of residence from birth to age 18 years were geocoded (latitude and longitude) and assigned UVB values using NASA's Total Ozone Mapping Spectrometer (TOMS) dataset. Linear regression was used to explore the relationship between cumulative UVB exposure (measured for age periods 0-6, 7-12, 13-18, 0-12, and 0-18) and age at MS onset. RESULTS: 3226 patients were included in the analysis. Of these, 74% were female, with an overall mean symptom onset age of 33.3 years. At onset, a total of 2944 (91%) had a relapsing-remitting disease course, 254 (8%) had primary progressive and the disease course for 28 (1%) was unknown. No significant associations between cumulative early life ambient UVB exposure and age at MS onset were observed. Patient sex, MS phenotype, and immigration to Canada after age 18 were significantly associated with age of onset (p < 0.01). CONCLUSIONS: Early life ambient UVB, as measured by satellite imagery, was not significantly associated with the age at MS onset. PMID: 29455071 [PubMed - indexed for MEDLINE]