한국환경과학회지 제29권 제3호 (p.249-255)

|ORIGINAL ARTICLE|
미세먼지의 di(2-ethylhexyl) phthalate가 유도한 피부상피세포 사멸 신호전달기전 연구

Di(2-ethylhexyl) Phthalate Induces the Apoptotic Cell Death Mediated by Production of Reactive Oxygen Species in Human Keratinocyte
키워드 :
Di(2-ethylhexyl) phthalate,Extracellular signal-regulated kinase,Skin keratinocyte,Nuclear factor-kappa B,Reactive oxygen species

목차

Abstract
1. 서 론
2. 재료 및 방법
   2.1. 시약
   2.2. 세포 배양
   2.3. 세포생존율 측정
   2.4. 세포 내 활성산소량 측정
   2.5. Western blot 분석
   2.6. 통계처리
3. 결과 및 고찰
   3.1. 프탈레이트가 피부상피세포 생존율에 미치는 영향
   3.2. 피부상피세포 활성산소종 생성에 있어서 프탈레이트가 미치는 영향
   3.3. 프탈레이트에 의한 피부상피세포 MAPKs의 활성변화
   3.4. 프탈레이트에 의한 NF-κB의 활성 변화
   3.5. 피부상피세포의 사멸을 유도하는 caspase-3의 활성에 있어서 프탈레이트가 미치는 영향
4. 결 론
REFERENCES

초록

Particulate matter with an aerodynamic diameter of less than 2.5 μM (PM2.5) is one of the major environmental pollutants. Di(2-ethylhexyl) phthalate (DEHP), an endocrine disrupting chemical in PM2.5, has been utilized for the manufacturing of polyvinyl chloride to increase the flexibility of final products. In the present study, we investigated the ecotoxicological effect of DEHP on the viability of skin keratinocytes (HaCaT). DEHP induced apoptotic cell death mediated by phosphorylation of extracellular signal-regulated kinase through the production of intracellular Reactive Oxygen Species (ROS). Interestingly, we found that DEHP induces the phosphorylation of the nuclear factor-kappa B responsible for the expression of cleaved caspase-3 as an executional cell death protease in HaCaT cells. On the basis of these results, we suggest that DEHP in PM2.5 induces the apoptotic death of human keratinocytes via ROS-mediated signaling events.