{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T01:02:38Z","timestamp":1790470958296,"version":"4.1.0"},"reference-count":38,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2006,1,24]],"date-time":"2006-01-24T00:00:00Z","timestamp":1138060800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Photoderm Photoimm Photomed"],"published-print":{"date-parts":[[2006,2]]},"abstract":"<jats:p> <jats:italic>In vitro<\/jats:italic> and <jats:italic>in vivo<\/jats:italic> studies provide a body of evidence that adequate protection of the skin against ultraviolet (UV)\u2010induced damage requires photostable broad\u2010spectrum sunscreens with a proper level of UVA protection. UVA alone and UV solar simulated radiation (SSR) induce DNA lesions in keratinocytes and melanocytes as reflected by the comet assay and p53 accumulation. UVA and SSR impair the immune system as shown by significant alteration of Langerhans cells and inhibition of contact hypersensitivity response to chemical allergens and delayed\u2010type hypersensitivity response to recall antigens. Any of these detrimental effects is more efficiently prevented by sunscreens with a higher level of protection in the UVA range. The involvement of UVA (fibroblast alteration, increased metalloproteinase expression) and the pivotal need for well\u2010balanced UVA\/UVB sunscreens were further demonstrated using reconstructed three\u2010dimensional skin models.<\/jats:p>","DOI":"10.1111\/j.1600-0781.2006.00188.x","type":"journal-article","created":{"date-parts":[[2006,1,24]],"date-time":"2006-01-24T13:21:53Z","timestamp":1138108913000},"page":"22-32","source":"Crossref","is-referenced-by-count":54,"title":["Protection of skin biological targets by different types of 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