UVA-induced immunosuppression

Halliday, Gary M.; Bestak, Rosa; Yuen, Kylie S.; Cavanagh, Lois L.; Barnetson, Ross StC

doi:10.1016/s0027-5107(98)00185-7

Cited by 56 publications

(47 citation statements)

References 13 publications

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“…This reversibility would allow for prophylactic pharmacologic interventions in high-risk patient groups (e.g., immunosuppressed patients) to try and prevent CSCC formation. In this regard, the earlier reports that vitamin E can inhibit UV-induced SCC formation are entirely consistent with the results of the present study and also support the thesis that an increased peroxidative burden may contribute to UV-induced SCC formation (41,42).…”

Section: Discussionsupporting

confidence: 93%

“…The present study now provides the first direct evidence that disruptions to peroxide and ROS metabolism are direct contributors to UV-induced SCC. Such a conclusion is entirely consistent with earlier studies, which showed that elevated peroxide levels and peroxide-derived reactive intermediates were associated with UV-induced skin cancers (14,21) and that antioxidants, such as vitamin E, can inhibit UV-induced CSCC formation (41,42). Although UV irradiation is known to induce elevations in ROS and the ROS-dependent 7,8-dihydroxyguanine DNA adduct in skin and CSCC, there is growing acceptance that this is predominantly due to the UVA wavelength component of UV irradiation (35,(43)(44)(45).…”

Section: Discussionsupporting

confidence: 92%

“…This would also suggest that, although the GPX2 enzyme affords protection from UVA damage, it may not be protective against UVB-induced effects (43) on CSCC formation. Interestingly, UVA and UVB are known to modulate local and systemic immune function (41,45). Thus, the predisposition of Gpx2-deficient mice to UV-induced carcinoma formation may be attributable to defects in the keratinocytes as well as other cell types.…”

Section: Discussionmentioning

confidence: 99%

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Inactivation of Glutathione Peroxidase Activity Contributes to UV-Induced Squamous Cell Carcinoma Formation

et al. 2007

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Cutaneous squamous cell carcinomas (CSCC) are a common malignancy of keratinocytes that arise in sites of the skin exposed to excessive UV radiation. In the present study, we show that human SCC cell lines, preneoplastic solar keratoses (SK), and CSCC are associated with perturbations in glutathione peroxidase (GPX) activity and peroxide levels. Specifically, we found that two of three SKs and four of five CSCCs, in vivo, were associated with decreased GPX activity and all SKs and CSCCs were associated with an elevated peroxide burden. Given the association of decreased GPX activity with CSCC, we examined the basis for the GPX deficiency in the CSCCs. Our data indicated that GPX was inactivated by a posttranslational mechanism and that GPX could be inactivated by increases in intracellular peroxide levels. We next tested whether the decreased peroxidase activity coupled with an elevated peroxidative burden might contribute to CSCC formation in vivo. This was tested in Gpx1 À/À and Gpx2 À/À mice exposed to solar-simulated UV radiation. These studies showed that Gpx2 deficiency predisposed mice to UV-induced CSCC formation. These results suggest that inactivation of GPX2 in human skin may be an early event in UV-induced SCC formation. [Cancer Res 2007;67(10):4751-8]

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

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Inactivation of Glutathione Peroxidase Activity Contributes to UV-Induced Squamous Cell Carcinoma Formation

et al. 2007

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“…22 UV radiation can induce both, local and systemic immunosuppression. 41,42 One of the mechanisms by which UV-A affects biological systems is production of reactive oxygen species 43,44 by upregulation of the heme-catabolizing enzyme and heme-oxygenase-1. There is also evidence that this enzyme is responsible for the UV-A mediated protection against UV-B-induced immunosuppression that occurs in skin.…”

Section: Biological Plausibilitymentioning

confidence: 99%

Sun exposure and malignant lymphoma: A population‐based case–control study in Germany

Weihkopf

Becker

Nieters

et al. 2007

Intl Journal of Cancer

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Although some causes for malignant lymphoma are known their etiology is not well understood so far. We analyze the relationship between sun exposure and malignant lymphoma in a multicenter, population-based case-control study. Patients with malignant lymphoma (n 5 710, 18-80 years) were prospectively recruited in 6 study regions in Germany. For each case, a gender, region and age-matched control was drawn from population-registers. In personal interviews, lifetime holidays spent in sunny climate, outdoor leisure activities and sunbed or sunlamp use were recorded. On basis of job task-specific supplementary questionnaires, an occupational physician assessed the cumulative working time outside. Odds ratios (OR) and 95%-confidence-intervals (CI) were calculated using conditional logistic regression analysis, adjusted for smoking and alcohol consumption. To increase statistical power, patients with specific lymphoma subentities were additionally compared with the entire control group using unconditional logistic regression. We observed a reduced overall lymphoma risk among subjects having spent vacations at sunny climates or frequently used sunbeds or sunlamps. The analysis of lymphoma subentities revealed similar results with the exception of T-NHL and follicular lymphoma which were positively associated with outdoor leisure activities. While cumulative working time outside appeared unrelated to NHL overall and most subentities, it was negatively associated with follicular lymphoma and weakly positively to HL. This data suggest that exposure to natural and artificial ultraviolet radiation may reduce the OR for lymphoma in this study population. ' 2007 Wiley-Liss, Inc.

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“…The corrected analysis showed that the best of the sunscreens could only provide approximately 50% of their SPF values for immune protection (57). Thus, it can be safely assumed that a portion of the action spectrum for solar immune suppression lies beyond the UVB region and in the UVA region (58). How far into the UVA spectrum skin needs to be protected to prevent immune suppression is unknown at this time.…”

Section: P53 Induction and Mutations In Physiologically Nonnal Skin Amentioning

confidence: 99%

Sunscreens, skin photobiology, and skin cancer: the need for UVA protection and evaluation of efficacy.

Gasparro

2000

Environ Health Perspect

108

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Sunscreens are ultraviolet radiation (UVR)-absorbing chemicals that attenuate the amount and nature of UVR reaching viable cells in the skin. They are selected and tested for their ability to prevent erythema. No sunscreen prevents photodamage, as it has been demonstrated that suberythemal doses of UVR cause a variety of molecular changes (including DNA damage) in these cells. Furthermore, the spectrum of UVR reaching viable cells is altered by topically applied sunscreen. In this review, the basic aspects of sunscreens and skin photobiology are reviewed briefly. Although there can be no question concerning the efficacy of sunscreens for the prevention of erythema, questions remain because of the possible cumulative effects of chronic suberythemal doses and the increased exposure of skin cells to longer UVR wavelengths. The current major issue surrounding sunscreens involves their ability to protect skin cells against the effects of UVA radiation. These UVA effects may be direct damage (base oxidations) or effects on the skin immune system, yet there is no uniformly accepted method for the evaluation of UVA protection. This review is focused primarily on the latter topic covering action spectra that implicate the need for UVA protection. In addition, in vivo and in vitro methods proposed for the evaluation of candidate sunscreen formulations of UVA protective ability are reviewed. Finally, revisions in the terminology used to describe the protection afforded by sunscreens are suggested. It is proposed that SPF ("sun" protection factor) be renamed "sunburn" protection factor and that "critical wavelength" be designated "long wave index." Key words: critical wavelength, long wave index, sun protection factor, sunburn protection factor, ultraviolet radiation. -Environ Health Perspect 108 (suppl 11:71-78 (2000).http.//ehpnetl.niehs.nih.gov/docs/2000/suppl-1/71-78gasparro/abstract.html

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UVA-induced immunosuppression

Cited by 56 publications

References 13 publications

Inactivation of Glutathione Peroxidase Activity Contributes to UV-Induced Squamous Cell Carcinoma Formation

Inactivation of Glutathione Peroxidase Activity Contributes to UV-Induced Squamous Cell Carcinoma Formation

Sun exposure and malignant lymphoma: A population‐based case–control study in Germany

Sunscreens, skin photobiology, and skin cancer: the need for UVA protection and evaluation of efficacy.

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