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- 주제어 : N-bis(2-hydroxypropyl)nitrosamine (DHPN) (검색결과 1 건)
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극 저주파 전자기장이 N-bis(2-hydroxypropyl)nitrosamine과 Sulfadimethoxine에 의해 유발된 갑상샘 암에 미치는 영향
이수환(Soo Hwan Lee),박용진(Young Jin Park),박언섭(Eon Sub Park),김용석(Young Seok Kim),최유신(Yoo Shin Choi),김범규(Beom Gyu Kim),박성준(Sung Jun Park),정세민(Se Min Chong) 대한외과학회 2009 Annals of Surgical Treatment and Research(ASRT) Vol.77 No.3
Purpose: Long-term exposure to extremely low-frequency (60 ㎐) electromagnetic fields (ELF-EMF) raises the questions of the induction of biological effects including tumorigenesis. One mechanism through which ELF-MFS could influence neoplastic development is the imbalance of cellular proliferation and cell apoptosis. The present study investigated the effect of ELF-EMF on chemically-induced thyroid carcinogenesis in a rat. Methods: We examined cellular proliferation index measured by anti-Ki-67 antigen, apoptosis, apoptosis related proteins such as caspase 3 and p53, and cell cycle-related proteins (cyclin D1 and p21<SUP>WAF1</SUP>/Cip1). Forty Male F344 rats received a subcutaneous N-bis(2-hydroxypropyl)nitrosamine (DHPN, 2,800 ㎎/㎏) injection, and 1 week later were allowed free access to drinking water containing sulfadimethoxine (0.1%) for 12 weeks. Twenty rats were exposed by ELF-EMF. During the carcinogenesis, sequential histological changes from hyperplasia, adenoma, and ultimately to overt carcinomas were noted. Results: The exposure group of ELF-EMF, significantly increases the number size of carcinomas. Also, the proliferative and apoptotic indices were significantly increased in the ELF-EMF exposure group than in the control group. The caspase 3 protein expression did not show any significant changes between ELF-EMF group and control group. The p53 protein was not detected in both ELF-EMF exposure and control group. Among the cell cycle related proteins, cyclin D1, not p21<SUP>WAF1</SUP>/Cip1, was significantly increased in adenomas and carcinomas in ELF-EMF exposure group compared with the control group. Conclusion: Exposure of ELF-EMF effects on chemically-induced rat thyroid carcinogenesis as results of altered increase of cellular proliferation, apoptosis, and cyclin D1 expression.
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