作者: Eric J. Song , Clare Gordon-Thomson , Louise Cole , Harvey Stern , Gary M. Halliday
DOI: 10.1016/J.JSBMB.2012.11.003
关键词: Oxidative stress 、 Photoprotection 、 Biochemistry 、 Reactive nitrogen species 、 Pyrimidine dimer 、 Sunburn 、 8-Hydroxy-2'-deoxyguanosine 、 Chemistry 、 DNA damage 、 Human skin
摘要: Vitamin D production requires UVB. In turn, we have shown that vitamin compounds reduce UV-induced damage, including inflammation, sunburn, thymine dimers, the most frequent type of cyclobutane pyrimidine dimer, immunosuppression, and photocarcinogenesis. Our previous studies photoprotective effects by 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3) occurred through nongenomic pathway because similar protection was seen with an analog, 1α,25-dihydroxylumistrol3 (JN), which has little ability to alter gene expression also a antagonist 1,25(OH)2D3 abolished protection. current study, tested whether this effect would extend other types DNA could be demonstrated in human ex vivo skin, as model suited pre-clinical testing topical formulations for photoprotection. particular, using skin explants, examined time course dimers (TDs), abundant photolesion, well 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), is mutagenic base lesion arising from oxidative stress, 8-nitroguanosine (8-NG). Nitric oxide products, known markers chronic inflammation carcinogenesis, are induced UV. This study showed significantly reduced TD 8-NG early 30min post UV, 8-oxodG at 3h confirming against photoproducts explants. At least part, mechanism photoprotection likely reduction reactive nitrogen species subsequent nitrosative damage. article part Special Issue entitled 'Vitamin Workshop'.