A new hair follicle-derived human epidermal model for the evaluation of sunscreen genoprotection

Bacqueville, Daniel; Douki, Thierry; Duprat, L.; Rebelo-Moreira, Silvestre; Guiraud, B.; Dromigny, H.; Perier, V.; Bessou‐Touya, S.; Duplan, Hélène

doi:10.1016/j.jphotobiol.2015.06.015

Cited by 32 publications

(38 citation statements)

References 52 publications

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“…There was also a comparable induction of 6-4PP and their Dewar valence isomers on the various treatment sites. The respective photoproduct yields in the acute 4 SED positive controls agree with previous reports in skin exposed to UVB (280-315 nm) (21,22) and SSR (34), which show fewer 6-4PP and their Dewar valence isomers than CPD, and that the Dewar TC derivatives are more frequent than the TT. Furthermore, we report here for the first time, the presence of Dewar isomers in human skin exposed in vivo to SSR.…”

Section: Repeated Exposure Groupsupporting

confidence: 90%

Sub-optimal Application of a High SPF Sunscreen Prevents Epidermal DNA Damage in Vivo

et al. 2018

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The cyclobutane pyrimidine dimer (CPD) is a potentially mutagenic DNA photolesion that is the basis of most skin cancers. There are no data on DNA protection by sunscreens under typical conditions of use. The study aim was to determine such protection, in phototypes I/II, with representative sunscreen-user application. A very high SPF formulation was applied at 0.75, 1.3 and 2.0 mg/cm2. Unprotected control skin was exposed to 4 standard erythema doses (SED) of solar simulated UVR, and sunscreen-treated sites to 30 SED. Holiday behaviour was also simulated by UVR exposure for 5 consecutive days. Control skin received 1 SED daily, and sunscreen-treated sites received 15 (all 3 application thicknesses) or 30 (2.0 mg/cm2) SED daily. CPD were assessed by quantitative HPLC-tandem mass spectrometry (HPLC-MS/MS) and semi-quantitative immunostaining. In comparison with unprotected control sites, sunscreen significantly (p ≤ 0.001-0.05) reduced DNA damage at 1.3 and 2.0 mg/cm2 in all cases. However, reduction with typical sunscreen use (0.75 mg/cm2) was non-significant, with the exception of HPLC-MS/MS data for the 5-day study (p <0.001). Overall, these results support sunscreen use as a strategy to reduce skin cancer, and demonstrate that public health messages must stress better sunscreen application to get maximal benefit.

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Section: Repeated Exposure Groupsupporting

confidence: 90%

Sub-optimal Application of a High SPF Sunscreen Prevents Epidermal DNA Damage in Vivo

et al. 2018

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“…Considering that the fluence of UVA is 20 times larger than that of UVB in sunlight, it may be estimated to be at the origin of a few percent of the overall load of DNA damage. It has been unambiguously shown by different assays that CPD, but not 64PP or Dewar, were efficiently produced by UVA in human cells and skin (37,(50)(51)(52). CPD is now known to be the most frequent photodamage in the UVA range (32,37,53,54).…”

Section: Uv-induced Dna Damage In Melanocytesmentioning

confidence: 99%

Oxidative Stress and Genotoxicity in Melanoma Induction: Impact on Repair Rather Than Formation of DNA Damage?

Douki

2020

Photochem & Photobiology

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Keratinocytes and melanocytes, two cutaneous cell types located within the epidermis, are the origin of most skin cancers, namely carcinomas and melanomas. These two types of tumors differ in many ways. First, carcinomas are almost 10 times more frequent than melanomas. In addition, the affected cellular pathways, the mutated genes and the metastatic properties of the tumors are not the same. This review addresses another specificity of melanomas: the role of photo‐oxidative stress. UVA efficiently produces reactive oxygen species in melanocytes, which results in more frequent oxidatively generated DNA lesions than in other cell types. The question of the respective contribution of UVB‐induced pyrimidine dimers and UVA‐mediated oxidatively generated lesions to mutagenesis in melanoma remains open. Recent results based on next‐generation sequencing techniques strongly suggest that the mutational signature associated with pyrimidine dimers is overwhelming in melanomas like in skin carcinomas. UVA‐induced oxidative stress may yet be indirectly linked to the genotoxic pathways involved in melanoma through its ability to hamper DNA repair activities.

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“…For each volunteer, sunscreen was applied at 2 mg/cm 2 on the interior of one forearm, [15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30] minutes before exposure to SSR. The other forearm was left untreated.…”

Section: Irradiation Procedures and Collection Of The Suction Blistersmentioning

confidence: 99%

“…Most available data have been obtained by antibody-based approaches such as immunohistochemistry, immunodot blot or radio immunoassays [17][18][19][20][21][22][23][24]. Data on photoprotection were also obtained on the basis of chromatographic assay [25,26]. The advantage of the latter approach is that results are quantitative and that individual results are provided on each of the possible bipyrimidic photoproducts [27].…”

Section: Introductionmentioning

confidence: 99%

The use of suction blisters to measure sunscreen protection against UVR-induced DNA damage

Josse

Douki

Digabel

et al. 2018

Journal of Photochemistry and Photobiology B: Biology

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The formation of DNA photoproducts caused by solar UVR exposure needs to be investigated in-vivo and in particular in order to assess sunscreens' level of protection against solar genotoxicity. The study's purposes were: i) to evaluate if the roof of suction blisters is an appropriate sampling method for measuring photoproducts, and ii) to measure in-vivo sunscreen protection against cyclobutane pyrimidine dimers. Skin areas on the interior forearms of eight healthy volunteers were exposed in-vivo to 2 MED of simulated solar radiation (SSR) and to 15 MED on a sunscreen protected area. After irradiation, six suction blisters were induced and the blister roofs were collected. Analysis of SSR-induced CPDs was performed by two independent methods: a chromatography coupled to mass spectroscopy (HPLC-MS/MS) approach and a 3D-imaging of CPD immunostaining by multiphoton microscopy on floating epidermal sheets. HPLC-MS/MS analyses showed that SSR-unexposed skin presented no CPD dimers, whereas 2 MED SSR-exposed skin showed a significant number of TT-CPD. The sunscreen covered skin exposed to 15 MED appeared highly protected from DNA damage, as the amount of CPD-dimers remained below the detection limit. The multiphoton-immunostaining analysis consistently showed that no CPD staining was observed on the non-SSR-exposed skin. A significant increase of CPD staining intensity and number of CPD-positive cells were observed on the 2 MED SSR-exposed skin. Sunscreen protected skin presented a very low staining intensity and the number of CPD-positive cells remained very close to non-SSR-exposed skin. This study showed that suction blister samples are very appropriate for measuring CPD dimers in-vivo, and that sunscreens provide high protection against UVR-induced DNA damage.

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A new hair follicle-derived human epidermal model for the evaluation of sunscreen genoprotection

Cited by 32 publications

References 52 publications

Sub-optimal Application of a High SPF Sunscreen Prevents Epidermal DNA Damage in Vivo

Sub-optimal Application of a High SPF Sunscreen Prevents Epidermal DNA Damage in Vivo

Oxidative Stress and Genotoxicity in Melanoma Induction: Impact on Repair Rather Than Formation of DNA Damage?

The use of suction blisters to measure sunscreen protection against UVR-induced DNA damage

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