Green H A, Margolis R, Boll J, Kochevar I E, Parrish J A, Oseroff A R
J Invest Dermatol. 1987 Aug;89(2):201-4. doi: 10.1111/1523-1747.ep12470562.
DNA damage repaired by the excision repair system and measured as unscheduled DNA synthesis (UDS) was assessed in freshly excised human skin after 193 and 248 nm ultraviolet (UV)-excimer laser ablative incisions. Laser irradiation at 248 nm induced DNA damage throughout a zone of cells surrounding the ablated and heat-damaged area. In contrast, with 193 nm irradiation UDS was not detected in cells adjacent to the ablated area, even though DNA strongly absorbs this wavelength. Our results suggest that the lack of UDS after 193 nm irradiation is due to: "shielding" of DNA by the cellular interstitium, membrane, and cytoplasm, DNA damage that is not repaired by excision repair, or thermal effects that either temporarily or permanently inhibit the excision repair processes.
在193和248纳米紫外准分子激光消融切口后,对新鲜切除的人体皮肤中通过切除修复系统修复并以非预定DNA合成(UDS)衡量的DNA损伤进行了评估。248纳米的激光照射在消融和热损伤区域周围的细胞区域诱导了DNA损伤。相比之下,尽管DNA强烈吸收193纳米波长,但在消融区域相邻的细胞中未检测到UDS。我们的结果表明,193纳米照射后缺乏UDS是由于:细胞间质、细胞膜和细胞质对DNA的“屏蔽”、切除修复无法修复的DNA损伤,或暂时或永久抑制切除修复过程的热效应。