Dewar valence isomers, the third type of environmentally relevant DNA photoproducts induced by solar radiation

Douki, Thierry; Sage, Évelyne

doi:10.1039/c5pp00382b

Cited by 47 publications

(49 citation statements)

References 67 publications

(94 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Interestingly, only small quantities of (6-4) photoproducts form at wavelengths between 300 and 305 nm and this level further diminishes at longer wavelengths . A fraction of the (6-4)PPs can be converted to their Dewar valence isomers by the absorption of a photon in the 320 nm range leading to the formation of a lesion that is potentially more mutagenic than its parent product (Douki and Sage 2016). The sunlight wavelengths that reach the earth's surface are strongly diminished below 300 nm.…”

Section: Uv-induced Dna Damage Formationmentioning

confidence: 99%

Mechanisms of UV-induced mutations and skin cancer

Pfeifer

2020

GENOME INSTAB. DIS.

View full text Add to dashboard Cite

Ultraviolet (UV) irradiation causes various types of DNA damage, which leads to specific mutations and the emergence of skin cancer in humans, often decades after initial exposure. Different UV wavelengths cause the formation of prominent UV-induced DNA lesions. Most of these lesions are removed by the nucleotide excision repair pathway, which is defective in rare genetic skin disorders referred to as xeroderma pigmentosum. A major role in inducing sunlight-dependent skin cancer mutations is assigned to the cyclobutane pyrimidine dimers (CPDs). In this review, we discuss the mechanisms of UV damage induction, the genomic distribution of this damage, relevant DNA repair mechanisms, the proposed mechanisms of how UV-induced CPDs bring about DNA replication-dependent mutagenicity in mammalian cells, and the strong signature of UV damage and mutagenesis found in skin cancer genomes.Keywords Ultraviolet · UV · Cyclobutane pyrimidine dimer · (6-4) Photoproduct · Mutations · DNA repair · Skin cancer · Melanoma Abbreviations UV light Ultraviolet light CPD Cyclobutane pyrimidine dimer (6-4)PP Pyrimidine (6-4) pyrimidone photoproduct 8-oxo-dG 8-Oxo-7,8-dihydro-2′-deoxyguanosine XP Xeroderma pigmentosum NER Nucleotide excision repair 5mC 5-Methylcytosine

show abstract

Section: Uv-induced Dna Damage Formationmentioning

confidence: 99%

Mechanisms of UV-induced mutations and skin cancer

Pfeifer

2020

GENOME INSTAB. DIS.

View full text Add to dashboard Cite

show abstract

“…It is important to mention that 6-4 PP undergo Dewar isomerization, to form a new photoproduct, which is repaired by NER. In fact, upon exposure to sunlight, UVA radiation converts the 6-4 PP into Dewar PP (Clingen et al, 1995;Perdiz et al, 2000;Douki et al, 2003;Douki and Sage, 2016).…”

Section: Dna Glycosylase Neil1 Binds and Excises Psoraleninduced Monomentioning

confidence: 99%

Cooperation and interplay between base and nucleotide excision repair pathways: From DNA lesions to proteins

et al. 2020

View full text Add to dashboard Cite

Base and nucleotide excision repair (BER and NER) pathways are normally associated with removal of specific types of DNA damage: small base modifications (such as those induced by DNA oxidation) and bulky DNA lesions (such as those induced by ultraviolet or chemical carcinogens), respectively. However, growing evidence indicates that this scenario is much more complex and these pathways exchange proteins and cooperate with each other in the repair of specific lesions. In this review, we highlight studies discussing the involvement of NER in the repair of DNA damage induced by oxidative stress, and BER participating in the removal of bulky adducts on DNA. Adding to this complexity, UVA light experiments revealed that oxidative stress also causes protein oxidation, directly affecting proteins involved in both NER and BER. This reduces the cell's ability to repair DNA damage with deleterious implications to the cells, such as mutagenesis and cell death, and to the organisms, such as cancer and aging. Finally, an interactome of NER and BER proteins is presented, showing the strong connection between these pathways, indicating that further investigation may reveal new functions shared by them, and their cooperation in maintaining genome stability.

show abstract

“…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%

“…2). Another interesting feature is that of 64PPs and their Dewar valence isomers which result from the conversion of UVB-induced 64PPs by the UVA portion of the simulated sunlight spectrum [15,30] were detected only in minute amounts close to the detection limit in only a few samples of unprotected irradiated skin.…”

Section: Quantification Of Photoproducts By Hplc-ms/msmentioning

confidence: 99%

“…UVA-induced 64PPs have been detected by immunological assays [8,12,13] but not by the more specific HPLC-MS/MS technique [10,11,14]. Evidence has also been provided for a major role of UVA in conversion of UVBinduced 64PPs into their Dewar valence isomers [15]. Interestingly, CPDs are induced in larger yield than 8-oxoGua in human skin and cells exposed to UVA [10,14,16].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

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

View full text Add to dashboard Cite

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.

show abstract

Dewar valence isomers, the third type of environmentally relevant DNA photoproducts induced by solar radiation

Cited by 47 publications

References 67 publications

Mechanisms of UV-induced mutations and skin cancer

Mechanisms of UV-induced mutations and skin cancer

Cooperation and interplay between base and nucleotide excision repair pathways: From DNA lesions to proteins

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

Contact Info

Product

Resources

About