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디펩타이드의 B16 악성흑색종세포에서 멜라닌 생성억제작용
남희승 ( Hee Seung Nam ),김은현 ( Eun-hyun Kim ),김수연 ( Su Yeon Kim ),이현이 ( Hyun-e Lee ),홍지연 ( Jiyun Hong ),이재국 ( Jae Guk Lee ),조성태 ( Sung Tai Cho ),조양환 ( Yang Hwan Cho ),윤혜영 ( Hye-young Yun ),백광진 ( Kwang Ji 대한화장품학회 2012 대한화장품학회지 Vol.38 No.1
본 연구에서는 B16 악성흑색종 세포에서 디펩타이드(dipeptide)의 멜라닌생성 저해 효과를 연구하였다. 실험결과 WV (트립토판-발린), WM (트립토판-메치오닌), CQ (시스테인-글루타민)는 멜라닌 생성을 농도 의존적으로 감소시켰다. 그러나 디펩타이드는 멜라닌 생합성과정의 속도 조절 단계 효소인 타이로시네이즈(tyrosinase)의 활성을 직접 감소시키지는 않았다. 따라서 타이로시네이즈의 발현양상을 조사하였고, 실험 결과 α-MSH가 유도한 타이로시네이즈 발현이 WV, WM, 그리고 CQ에 의해 억제되었다. 그러므로 WV, WM, 그리고 CQ가 타이로시네이즈의 억제성 조절(down-regulation)을 통해 멜라닌 생성을 감소시킨다고 제안될 수 있다. In the present study, we investigated the effects of dipeptides on melanogenesis in B16 melanoma cells. It was found that WV (Trp+Val), WM (Trp+Met), and CQ (Cys+Gln) decreased melanin production dosedependently. However, dipeptides did not directly inhibit tyrosinase activity, the rate-limiting melanogenic enzyme. Therefore, we further investigated the expression of tyrosinase. Our results showed that α-MSH-induced tyrosinase expression was down-regulated by WV, WM, and CQ. Thus, we propose that WV, WM, and CQ show hypopigmentary activity through tyrosinase down-regulation.
Adriamycin과 Dimethylbenzanthracene의 투여에 의한 Mouse간장에서의 산소 독성 효과
최지영,백광진,이희성 중앙대학교 의과대학 의과학연구소 1989 中央醫大誌 Vol.14 No.4
We studied the changes of the activities of superoxide dismutase (EC 1. 15. 1. 1, SOD) and catalase (EC 1. 11. 1. 6) and the production of superoxide radical in mice liver after application of adriamycin (ADM) and dimethylbenzanthracene (DMBA). Mice were injected subcutneously with ADM (5 or 10 mg/kg body weight for 16 days) followed by topical application of DMBA in dose of 20 mg/kg once a week for 4 times. The results were summarized as follows: 1. In all experimental groups, the activities of Cu, Zn-SOD and catalase showed lower level than those in the controls (p<0.01). 2. The activities of Mn-SOD in 4 weeks of ADM 5 mg/kg group and 3,4 and 6 weeks of ADM 10 mg/kg groups appeared to be lower than t se in t e controls (p<0.05, P<0.01). 3. Production of superoxide radical in all experimental groups increased in comparison with its control value (p<0.01). In conclusion, it seems likely that ADM and DMBA could decrease the activities of SOD and catalase which are one of the factors in the liver defence mechanism for the oxygen toxicity and increase the superoxide radical production. Therefore, oxygen toxicity may be developed in mouse liver by ADM and DMBA.