In vivo effect of UV-B on lymphocyte function

Morison, Warwick L.; Parrish, John A.; Bloch, Kurt J.; Krugler, Joel I.

doi:10.1111/j.1365-2133.1979.tb11880.x

Cited by 65 publications

(15 citation statements)

References 8 publications

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“…Available data involving UVB radiation in vivo, however, have yielded contradictory results. Lymphocyte proliferative responses increased, 31) decreased 32) or were unchanged 33) from those of un-exposed subjects. The reason for these conflicting results may be linked to the type of radiation source and/or other irradiation conditions, postirradiation period and sample collection.…”

Section: Discussionmentioning

confidence: 85%

Acute Exposure to Solar Simulated Ultraviolet Radiation Affects Oxidative Stress-Related Biomarkers in Skin, Liver and Blood of Hairless Mice

Svobodová

Galandáková

Šianská

et al. 2011

Biological & Pharmaceutical Bulletin

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Solar light is the main environmental factor implicated in various skin disorders. Extensive evidence supports the notion that the whole solar spectrum (UV, visible and infrared wavelengths) participates in skin cells damage.1) However, UV wavelengths are regarded as the most hazardous and most toxic. The sun is primarily a UVA source with an approximate terrestrial UVB content of about 5-10%. UVA (315-400 nm) penetrates deep into the skin. Approximately 80% of UVA reaches the dermal-epidermal junction and around 10% of UVA even reaches the hypodermis. UVA photons are less energetic than UVB and cause mainly indirect damage via increased generation of reactive oxygen and nitrogen species (RONS). These reactive species attack biomolecules resulting in several types of DNA damage (e.g. DNA single strand breaks, DNA interstrand cross-links and nucleotide base modifications), formation of oxidized fragments and products of lipids (e.g. lipid alkoxyl radicals, aldehydes, alkanes, lipid (hydro)peroxides and epoxides) and oxidatively modified proteins and saccharides. In contrast, incoming UVB (295-315 nm) is mostly absorbed by the epidermis (90%). UVB is directly absorbed by the aromatic heterocyclic bases of DNA. As a result of UVB photons absorption cyclobutane-pyrimidine dimers and pyrimidine-(6-4)-pyrimidone photoproducts are formed.2) Aromatic amino acids such as tryptophan and tyrosine also act as potent UVB radiation absorbers and their interaction with high energetic UVB photons leads to the generation of several derivatives. Of these, 6-formylindolo[3,2-b]carbazole (FICZ) has been recognized to have fundamental importance.3) Amino acid modification alters protein function as well as affects cellular signalling. However, the division between UVA and UVB is arbitrary and UVB participates in RONS production as well. 4)Skin cells are equipped with several non-enzymic (ascorbic acid, tocopherol, ubiquinol, and glutathione (GSH)) and enzymic antioxidants (catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPX)) that maintain the prooxidant/antioxidant balance by rapid RONS elimination, resulting in cell and tissue stabilization. However, flooding of reactive species causes antioxidants depletion and further formation of reactive products that both result in oxidative stress. Production of modified biomolecules is also accompanied by alteration to various enzyme activity and regulation of gene expression in several pathways such as inflammatory cytokines, mitogen-activated protein kinases, matrix metalloproteinases, nuclear factor-kB, nuclear factor erythroid-2 related factor 2 (Nrf2) and phase 2 detoxifying enzymes such as nicotinamide adenine dinucleotide (phosphate) quinone oxidoreductase (NQO1), hem oxygenase-1 (HO-1), glutathione transferase (GST) and glutathione reductase (GSR). 4,5) Over 50 years of UV light research, a number of authors have examined the effects of chronic and/or repeated exposures. However, lacking of number reports has pursued the acute effects of UVA/UVB exposure. [6][7][...

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Section: Discussionmentioning

confidence: 85%

Acute Exposure to Solar Simulated Ultraviolet Radiation Affects Oxidative Stress-Related Biomarkers in Skin, Liver and Blood of Hairless Mice

Svobodová

Galandáková

Šianská

et al. 2011

Biological & Pharmaceutical Bulletin

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“…Furthermore, the ultraviolet B (UVB) component of sunlight (same wavelengths, 290–320 nm, used to induce SCC in the present model) is a complete carcinogen and is responsible for most non-melanoma skin cancers [37], [38]. Importantly, SCCs are immunogenic and can be eliminated by endogenous cell-mediated immune responses [39]–[41], however, UV exposure suppresses lymphocyte trafficking, and T and NK cell function [42], and inhibits anti-SCC immunity [43]–[45], all of which may enable SCC tumors to escape immune clearance [25], [46]. In light of the importance of anxiety being generated during the diagnosis and treatment of cancer, and the global health relevance and scientific value of the skin cancer model under study, here we investigate endocrine (physiological indices of chronic stress burden), immune (indices of protective versus suppressive immune function in the tumor microenvironment), and tumor growth-promoting (VEGF) mechanisms mediating the effects of high- versus low-anxious behavioral phenotypes on tumor emergence and progression.…”

Section: Introductionmentioning

confidence: 94%

High-Anxious Individuals Show Increased Chronic Stress Burden, Decreased Protective Immunity, and Increased Cancer Progression in a Mouse Model of Squamous Cell Carcinoma

et al. 2012

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In spite of widespread anecdotal and scientific evidence much remains to be understood about the long-suspected connection between psychological factors and susceptibility to cancer. The skin is the most common site of cancer, accounting for nearly half of all cancers in the US, with approximately 2–3 million cases of non-melanoma cancers occurring each year worldwide. We hypothesized that a high-anxious, stress-prone behavioral phenotype would result in a higher chronic stress burden, lower protective-immunity, and increased progression of the immuno-responsive skin cancer, squamous cell carcinoma. SKH1 mice were phenotyped as high- or low-anxious at baseline, and subsequently exposed to ultraviolet-B light (1 minimal erythemal dose (MED), 3 times/week, 10-weeks). The significant strengths of this cancer model are that it uses a normal, immunocompetent, outbred strain, without surgery/injection of exogenous tumor cells/cell lines, and produces lesions that resemble human tumors. Tumors were counted weekly (primary outcome), and tissues collected during early and late phases of tumor development. Chemokine/cytokine gene-expression was quantified by PCR, tumor-infiltrating helper (Th), cytolytic (CTL), and regulatory (Treg) T cells by immunohistochemistry, lymph node T and B cells by flow cytometry, adrenal and plasma corticosterone and tissue vascular-endothelial-growth-factor (VEGF) by ELISA. High-anxious mice showed a higher tumor burden during all phases of tumor development. They also showed: higher corticosterone levels (indicating greater chronic stress burden), increased CCL22 expression and Treg infiltration (increased tumor-recruited immuno-suppression), lower CTACK/CCL27, IL-12, and IFN-γ gene-expression and lower numbers of tumor infiltrating Th and CTLs (suppressed protective immunity), and higher VEGF concentrations (increased tumor angiogenesis/invasion/metastasis). These results suggest that the deleterious effects of high trait anxiety could be: exacerbated by life-stressors, accentuated by the stress of cancer diagnosis/treatment, and mediate increased tumor progression and/or metastasis. Therefore, it may be beneficial to investigate the use of chemotherapy-compatible anxiolytic treatments immediately following cancer diagnosis, and during cancer treatment/survivorship.

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“…Experimental studies in mice show that UVB light penetrates the outer layer of the skin of mice as thymine dimers were detected in both epidermal and dermal cells after UVAB irradiation (9). Whole-body UVB exposure to humans results in a decreased proportion of circulating E rosette-forming lymphocytes and decreased incorporation of tritiated thymidine into the DNA of lympho- (10). In general, these data indicate the outer layer of epidermis is not an effective barrier against UVB light.…”

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confidence: 99%

Sunlight‐induced DNA damage in human mononuclear cells

et al. 2002

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In this study of 301 blood samples from 21 subjects, we found markedly higher levels of DNA damage (nonpyrimidine dimer types) in the summer than in the winter detected by single-cell gel electrophoresis. The level of DNA damage was influenced by the average daily influx of sunlight < 50 days prior to blood sampling. The 3 and 6 day periods before sampling influenced DNA damage the most. The importance of sunlight was further emphasized by a positive association of the DNA damage level to the amount of time the subjects had spent in the sun over a 3 day period prior to the sampling. The effect of sunlight was comparable to the interindividual variation, indicating that sunlight exposure and the individual's background were the two most important determinants for the basal level of DNA damage. Influence of other lifestyle factors such as exercise, intake of foods, infections, and age could not be detected. Our results suggest that sunlight penetrates the outer layer of the human epidermis and damages the DNA in mononuclear cells circulating in the vessels of the skin.

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In vivo effect of UV-B on lymphocyte function

Cited by 65 publications

References 8 publications

Acute Exposure to Solar Simulated Ultraviolet Radiation Affects Oxidative Stress-Related Biomarkers in Skin, Liver and Blood of Hairless Mice

Acute Exposure to Solar Simulated Ultraviolet Radiation Affects Oxidative Stress-Related Biomarkers in Skin, Liver and Blood of Hairless Mice

High-Anxious Individuals Show Increased Chronic Stress Burden, Decreased Protective Immunity, and Increased Cancer Progression in a Mouse Model of Squamous Cell Carcinoma

Sunlight‐induced DNA damage in human mononuclear cells

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