The Effect of Repeated Exposures to Low-Dose UV Radiation on the Apoptosis of Peripheral Blood Mononuclear Cells

Cebula, Barbara; Lesiak, Aleksandra; Sysa-Jędrzejowska, Anna; Norval, Mary; Robak, Tadeusz; Smolewski, Piotr

doi:10.1001/archdermatol.2008.574

Cited by 10 publications

(11 citation statements)

References 33 publications

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“…Caspase expression was not observed in WBCs following UV + R PRT, suggesting that these cells underwent an alternative caspase‐independent apoptotic pathway. Reports using varying doses of UV exposure suggested that WBCs generally undergo conventional apoptosis, that is, caspase activation, up regulation of GADD45α, CD95 (FAS/APO‐1), Bax, and/or p73, and poly–adenosine diphosphate ribose polymerase cleavage . There are, however, reports of caspase‐independent apoptosis occurring in WBCs in response to other stimuli, or in other cell types in response to UV exposure, providing some precedence for our findings .…”

Section: Discussionsupporting

confidence: 59%

“…21,22 UVB light induces apoptosis in many different mouse and human cell types by various mechanisms. [23][24][25][26][27][28][29][30] Different wavelengths and doses of UV light have different effects, with lower doses generally inducing apoptosis and higher doses inducing necrosis. 29 The cell death pathway induced also depends on the cell type and is related to the extent of DNA damage.…”

Section: Discussionmentioning

confidence: 99%

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Pathogen reduction with riboflavin and ultraviolet light induces a quasi‐apoptotic state in blood leukocytes

et al. 2019

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Pathogen reduction with riboflavin and ultraviolet light induces a quasi-apoptotic state in blood leukocytes ABBREVIATIONS: ANOVA = analysis of variance; CPDA-1 = citrate phosphate dextrose anticoagulant; EtOH = ethanol; MFI = median fluorescence intensity; MHC = major histocompatibility complex; PBMCs = peripheral blood mononuclear cells; PE = phycoerythrin; PI = propidium iodide; PRP = platelet-rich plasma; PRT = pathogen reduction treatment; PS = phosphatidylserine; UV = ultraviolet; UV + R = ultraviolet light and riboflavin.From the

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Section: Discussionsupporting

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Pathogen reduction with riboflavin and ultraviolet light induces a quasi‐apoptotic state in blood leukocytes

et al. 2019

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“…Apoptosis was monitored in healthy volunteers following whole body UVB or SSR with 0.7 personal minimal erythema dose (MED) on 10 consecutive days ( 10 ). The UVB exposure was equivalent to around 35 minutes outside on a clear sky day in mid-Europe around midday, and the SSR to 15 minutes under the same conditions.…”

Section: Effects Of Uvr On Pbmcsmentioning

confidence: 99%

“…It was enhanced in the PBMCs from the irradiated individuals, with SSR being more effective than UVB, possibly because the UVA emitted by the SSR can penetrate more effectively into the dermal microvasculature. In addition, SSR had a greater effect on reducing the expression of anti-apoptotic proteins while increasing that of pro-apoptotic proteins, leading to the suggestion that UVA induces apoptosis of lymphocytes via photosensitised oxygen radicals ( 10 ).…”

Section: Effects Of Uvr On Pbmcsmentioning

confidence: 99%

More Than Effects in Skin: Ultraviolet Radiation-Induced Changes in Immune Cells in Human Blood

Hart

Norval

2021

Front. Immunol.

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Cells of the skin and circulation are in constant two-way communication. Following exposure of humans to sunlight or to phototherapy, there are alterations in the number, phenotype and function of circulating blood cells. In this review, only data obtained from human studies are considered, with changes induced by UV radiation (UVR) exposure described for phagocytic leukocytes and peripheral blood mononuclear cells plus their component T and B cells, natural killer cells and dendritic cells. These immune modulations illustrate the potential of UVR to have therapeutic effects beyond the skin, and that sunlight exposure is an important environmental influence on human health.

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“…Furthermore, repeated UV radiation can cause DNA damage and apoptosis on human peripheral blood mononuclear cells, which indicate that sunlight exposure may cause internal diseases by affecting blood components. [37], [38] In addition, UV radiation is known to activate multiple signaling cascades, leading to inflammatory reactions. [39] Despite all of these possible pathways, the mechanisms of the association between actinic skin damage and mortality remain unclear.…”

Section: Discussionmentioning

confidence: 99%

Actinic Skin Damage and Mortality - the First National Health and Nutrition Examination Survey Epidemiologic Follow-up Study

Fei

et al. 2011

PLoS ONE

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BackgroundExposure to sunlight may decrease the risk of several diseases through the synthesis of vitamin D, whereas solar radiation is the main cause of some skin and eye diseases. However, to the best of our knowledge, the association of sun-induced skin damage with mortality remains unknown.Methodology/Principal FindingsSubjects were 8472 white participants aged 25–74 years in the First National Health and Nutrition Examination Survey Epidemiologic Follow-up Study. Cardiovascular disease mortality, cancer mortality, and all-cause mortality were obtained by either a death certificate or a proxy interview, or both. Actinic skin damage was examined and recorded by the presence and severity (absent, minimal, moderate, or severe) of overall actinic skin damage and its components (i.e., fine telangiectasia, solar elastosis, and actinic keratoses). Cox regression and Kaplan-Meier methods were applied to explore the associations. A total of 672 cancer deaths, 1500 cardiovascular disease deaths, and 2969 deaths from all causes were documented through the follow-up between 1971 and 1992. After controlling for potential confounding variables, severe overall actinic skin damage was associated with a 45% higher risk for all-cause mortality (95% CI: 1.22, 1.72; P<0.001), moderate overall skin damage with a 20% higher risk (95% CI: 1.08., 1.32; P<0.001), and minimal overall skin damage with no significant mortality difference, when compared to those with no skin damage. Similar results were obtained for all-cause mortality with fine telangiectasia, solar elastosis, and actinic keratoses. The results were similar for cancer and cardiovascular disease mortality.ConclusionsThe present study gives an indication of an association of actinic skin damage with cardiovascular disease, cancer and all-cause mortality in white subjects. Given the lack of support in the scientific literature and potential unmeasured confounding factors, this finding should be interpreted with caution. More independent studies are needed before any practical recommendations can be made.

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The Effect of Repeated Exposures to Low-Dose UV Radiation on the Apoptosis of Peripheral Blood Mononuclear Cells

Abstract: To investigate whether repeated exposures to low-dose UV or solar-simulated radiation induce apoptosis of peripheral blood mononuclear cells.

Cited by 10 publications

References 33 publications

Pathogen reduction with riboflavin and ultraviolet light induces a quasi‐apoptotic state in blood leukocytes

Pathogen reduction with riboflavin and ultraviolet light induces a quasi‐apoptotic state in blood leukocytes

More Than Effects in Skin: Ultraviolet Radiation-Induced Changes in Immune Cells in Human Blood

Actinic Skin Damage and Mortality - the First National Health and Nutrition Examination Survey Epidemiologic Follow-up Study

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