Science. Science. Nature. Mol. Cell Biol. Click on Request Permissions which will take you to the Copyright Clearance Centers Downloaded from cancerres.aacrjournals.org on September. American Association for Cancer Research. Conventional photoprotection by sunscreens is exclusively prophylactic in nature and of no value once DNA damage has occurred.When a dose of UVB radiation sufcient to induce erythema was administered to the skin of healthy subjects, signicant numbers of dimers were formed within epidermal cells.No reduction was observed if the liposomes were not lled with photolyase or if photoreactivating exposure preceded the application of lled liposomes.The UVB dose administered resulted in suppression of intercellular adhesion molecule, a molecule required for immunity and inammatory events in the epidermis.In addition, in subjects hypersensitive to nickel sulfate, elicitation of the hypersensitivity reaction in irradiated skin areas was prevented.Photolyaseinduced dimer repair completely prevented these UVB radiationinduced immunosuppressive purchase Sapitinib effects as well as erythema and sunburncell formation.These studies demonstrate that topical application of photolyase is effective in dimer reversal and thereby leads to immunoprotection.B ecause of increased leisure time, the grow ing popularity of staying outdoors, and of holidays in the sun, it has become more and more important to study the molecular and cellular ef fects that ultrav iolet radiation exposure to the sun exerts on human sk in. In this context, a critical obser vation has been the appreciation that the induction of DNA damage by ultrav ioletB is detrimental to human health.Among the DNA lesions induced by UVB irradiation, cyclobutane py rimidine dimers predominate.From recent an imal work, it has been concluded that dimers also contribute to photocarcinogenesis through suppression of the sk ins immune system, allow ing transformed cells to grow un impeded. Strategies directed at the prevention of detrimental ef fects resulting from dimers in human sk in are, thus, of paramount concern for human health.Sunscreens prov ide protection against erythema of human sk in through absorption or ref lection of UV radiation. Thiswidely used photoprotective approach, however, is not ef fective once damage to sk in cells has been generated af ter sun exposure.In healthy human sk in, cyclobutane py rimidine dimers are repaired through nucleotide excision repair.Dimerspecific photolyase is present in an active form in numerous prokar yotes and certain eukar yotes, including fish and marsupials.The ex istence of photoreactivation in humans is controversial.A lthough recent reports have presented ev idence of photoreactivating activ ity in human white blood cells, many negative reports have questioned the validity of these findings. Nineteen healthy, adult human volunteers were studied.Indiv iduals were of sk in type II or III, without a historyof chron ic disease, and not currently on medication.For all indiv iduals included in the study, the MED was in the normal range, and in particular, no abnormal reaction to UVB radiation was obser ved.To assess the ef fect of UVB radiation on intercellular adhesion molecule subsequently was exposed to MED of UVB radiation or shamirradiated.Nuclei of skin cells were counterstained with propidium iodide.Nuclear greenfluorescence in the epidermal cells proportional to the level of thymine dimers was assessed with a scanning laser microscope by using image processing and image analysis.