Freeman S E, Gange R W, Sutherland J C, Matzinger E A, Sutherland B M
J Invest Dermatol. 1987 Apr;88(4):430-3. doi: 10.1111/1523-1747.ep12469778.
Cyclobutyl pyrimidine dimers, measured as sites recognized by the dimer-specific ultraviolet (UV) endonuclease from Micrococcus luteus, were produced in DNA of human skin exposed in situ to UVA (320-400 nm) radiation. The dimer yields produced by a broadband UVA source, by broadband UVA filtered to remove all light of wavelength less than 340 nm, and by narrow band radiation centered at 365 nm were similar, indicating that UVA radiation, and not stray shorter wavelength radiation, was responsible for dimer production. The identity of the UVA-induced DNA lesions was confirmed as pyrimidine dimers by photoreactivation of approximately 100% of the endonuclease-sensitive sites in vitro with the 40,000 dalton Escherichia coli photoreactivating enzyme.
环丁基嘧啶二聚体，以被来自藤黄微球菌的二聚体特异性紫外线（UV）内切核酸酶识别的位点来衡量，在原位暴露于UVA（320 - 400nm）辐射的人类皮肤DNA中产生。由宽带UVA源、经滤光以去除所有波长小于340nm的光的宽带UVA以及以365nm为中心的窄带辐射产生的二聚体产量相似，这表明是UVA辐射而非杂散的较短波长辐射导致了二聚体的产生。通过用40000道尔顿的大肠杆菌光复活酶在体外对约100%的内切核酸酶敏感位点进行光复活，证实了UVA诱导的DNA损伤为嘧啶二聚体。
