Borska Lenka, Andrys Ctirad, Krejsek Jan, Palicka Vladimir, Vorisek Viktor, Hamakova Kvetoslava, Kremlacek Jan, Borsky Pavel, Fiala Zdenek
Institute of Pathological Physiology, Charles University in Prague, Faculty of Medicine in Hradec Kralove, Šimkova 870, 50038 Hradec Kralove, Czech Republic.
Institute of Clinical Immunology and Allergology, Charles University in Prague, Faculty of Medicine in Hradec Kralove, 50038 Hradec Kralove, Czech Republic.
J Dermatol Sci. 2016 Mar;81(3):192-202. doi: 10.1016/j.jdermsci.2015.12.010. Epub 2015 Dec 28.
Ultraviolet radiation (UVR) and crude coal tar (CCT) containing PAHs can accelerate the skin-aging process (SAP). However, UVR induces the formation of an important protective factor in SAP (vitamin D).
To determine the relation of SAP to selected risks and benefits of combined dermal exposure to UVR and coal tar (PAHs).
The study group consisted of patients with chronic stable plaque psoriasis and treated by Goeckerman therapy (GT; daily dermal application of UVR and 5% CCT ointment). The levels of urinary 1-hydroxypyrene (1-OHP), oxidative stress (DNA and RNA damage), genotoxic damage (chromosomal aberration in peripheral lymphocytes; ABC), 25-hydroxy-vitamin D [25(OH)D] and the PASI score were evaluated before and after GT.
Intensive dermal absorption of PAHs was confirmed by increased levels of 1-OHP (p<0.01). After the therapy, we found an increased level of oxidative stress (p<0.05), an increased level of genotoxic damage (ABC; p<0.001), a high efficiency of the treatment (p<0.001) and an elevated production of 25(OH)D (p<0.01). We also found a relationship between the duration of UVR and the genotoxic damage (p<0.01), vitD (p<0.05) and the PASI score (p<0.05). Furthermore, we found a relationship between oxidative stress and 25(OH)D (p<0.05) and between genotoxic damage and the PASI score (p<0.05).
Dermal exposure to UVR and coal tar (PAHs) enhances the level of oxidative stress and genotoxic damage and thus contributes to SAP. However, the exposure is very effective as a treatment and elevates the production of 25(OH)D, the protective factor in SAP. According to our results, UVR is probably a more hazardous factor in SAP.
紫外线辐射(UVR)和含有多环芳烃的粗煤焦油(CCT)可加速皮肤老化过程(SAP)。然而,UVR可诱导SAP中一种重要保护因子(维生素D)的形成。
确定SAP与皮肤联合暴露于UVR和煤焦油(多环芳烃)的特定风险和益处之间的关系。
研究组由慢性稳定斑块状银屑病患者组成,采用Goeckerman疗法(GT;每日皮肤应用UVR和5%CCT软膏)治疗。在GT治疗前后评估尿中1-羟基芘(1-OHP)水平、氧化应激(DNA和RNA损伤)、遗传毒性损伤(外周淋巴细胞染色体畸变;ABC)、25-羟基维生素D[25(OH)D]水平及银屑病面积和严重程度指数(PASI)评分。
1-OHP水平升高证实了PAHs的大量皮肤吸收(p<0.01)。治疗后,我们发现氧化应激水平升高(p<0.05)、遗传毒性损伤水平升高(ABC;p<0.001)、治疗效果显著(p<0.001)以及25(OH)D生成增加(p<0.01)。我们还发现UVR照射时长与遗传毒性损伤(p<0.01)、维生素D(p<0.05)及PASI评分(p<0.05)之间存在关联。此外,我们发现氧化应激与25(OH)D之间(p<0.05)以及遗传毒性损伤与PASI评分之间(p<0.05)存在关联。
皮肤暴露于UVR和煤焦油(多环芳烃)会提高氧化应激水平和遗传毒性损伤,从而促进SAP。然而,这种暴露作为一种治疗方法非常有效,且能提高25(OH)D的生成,25(OH)D是SAP中的保护因子。根据我们的研究结果,UVR在SAP中可能是一个更具危害性的因素。