Tang Nai-Jun, Liu Jing, Coenraads P J, Dong Li, Zhao Li-Jun, Ma Shi-Wei, Chen Xi, Zhang Chun-Mei, Ma Xiao-Ming, Wei Wen-Guo, Zhang Peng, Bai Zhi-Peng
The College of Environmental Science and Engineering, Nankai University, Weijin Road 94#, Tianjin 300071, China.
Toxicol Lett. 2008 Apr 1;177(3):182-7. doi: 10.1016/j.toxlet.2008.01.011. Epub 2008 Feb 5.
Occupational exposure to certain polychlorinated aromatic hydrocarbons such as dioxins has been suggested to cause chloracne which is a kind of skin disease. The molecular mechanisms of dioxin-mediated chloracne have not been clarified. It is possible that dioxins contribute to the pathogenesis through activation of aryl-hydrocarbon receptor (AhR)-mediated transcription and downstream genes such as CYP1A1, GSTA1 and TGF-alpha. The study on genes was through chloracne lesional skin, which has rarely been reported on previously. The expression levels of key genes, such as AhR, CYP1A1, GSTA1, c-fos and TGF-alpha in human epidermal tissue of chloracne cases and controls were detected by real-time PCR. Compared with controls, AhR, CYP1A1, GSTA1 and c-fos transactivations were significantly induced in the skins of chloracne patients who had long-term exposure to dioxins and dibenzofuranes. The TGF-alpha mRNA content of epidermal tissue was increased, but not significantly compared with controls. The study demonstrates that constitutive activation of the AhR pathway is probably a prerequisite of chloracne pathogenesis. The changes of genes expression may disturb normal proliferation and differentiation of human epidermis cells, and then lead to chloracne.
职业接触某些多氯代芳烃（如二噁英）已被认为会导致一种皮肤病——氯痤疮。二噁英介导氯痤疮的分子机制尚未阐明。二噁英可能通过激活芳烃受体（AhR）介导的转录及下游基因（如CYP1A1、GSTA1和TGF-α）来促进发病机制。对基因的研究是通过氯痤疮皮损皮肤进行的，此前鲜有相关报道。采用实时PCR检测氯痤疮病例和对照者人体表皮组织中AhR、CYP1A1、GSTA1、c-fos和TGF-α等关键基因的表达水平。与对照组相比，长期接触二噁英和二苯并呋喃的氯痤疮患者皮肤中AhR、CYP1A1、GSTA1和c-fos的反式激活显著诱导。表皮组织的TGF-α mRNA含量增加，但与对照组相比无显著差异。该研究表明，AhR途径的组成性激活可能是氯痤疮发病机制的一个先决条件。基因表达的变化可能会干扰人体表皮细胞的正常增殖和分化，进而导致氯痤疮。
