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N-Methyl-N-Nitrosourea 유도 자매염색분체교환생성과 DNA메칠화에 대한 Galangin의 억제효과
손수정(Soo Jung Sohn),김정한(Jung Han Kim),김영진(Young Jin Kim),허인회(In Hoe Huh),허문영(Moon Young Heo) 대한약학회 1995 약학회지 Vol.39 No.1
In order to evaluate the suppressive effects of galangin on the DNA damage induced by N-methyl-N-nitrosourea(MNU), in vitro sister chromatid exchange(SCE) test using Chinese Hamster ovary(CHO) cells was performed. Also the determinations of [3H] MNU-induced total DNA binding and methylated DNA were performed to find out the mechanism of action by galangin. MNU-induced SCEs were significantly decreased by simultaneous and pretreatment of galangin when S-9 mix was added only. In post-treatment, however, the MNU-induced SCEs were not decreased whether S-9 mix was added or not. [3H] MNU-induced total DNA binding was significantly inhibited by the treatment of galangin in calf thymus DNA and CHO cells. HPLC analysis of DNA hydrolysates shows that galangin caused a dose-dependant decrease in calf thymus DNA, but not significant decrease in CHO cells. These results suggest that the inhibition of galangin on the MNU-induced SCEs is due to the decrease of DNA binding and methylation with MNU. Therefore, galangin may be useful as a chemopreventive agent of alkylating agents.
생쥐 골수세포에서 아드리아마이신의 소핵생성에 미치는 N-마세틸시스테인의 억제효과
손수정(Su Jung Sohn),허인회(In Hoe Huh),최성규(Sung Gyu Choi),허문영(Moon Young Heo) 대한약학회 1993 약학회지 Vol.37 No.3
The anticlastogenic effect of N-acetylcysteine was tested in vivo in mouse bone-marrow micronucleus assay. The frequencies of micronuclei induced by adriamycin (5mg/kg i.p.) in bone marrow cells were decreased by the oral administration of N-acetylcysteine at 12 h before adriamycin injection. The observed suppressing effect was not a reflection of a delay in the formation of micronuclei by the cytotoxic effect of N-acetylcysteine. The anticlastogenic effects of SH compound including N-acetylcysteine, cysteine, cystine, S-carboxy methylcysteine and glutathione were also investigated by the multiple pretreatment. Each SH compound was administered orally every day for 5 days and adriamycin (5mg/kg i.p.) was injected at 24 h after the last dose of test compound. N-acetylcysteine and glutathione showed significantly the suppressive effect at dose of 10 and 25mg/kg for N-acetylcysteine and at the dose of 25mg/kg for glutathione. Our study suggests that N-acetylcysteine is capable of protecting the chromosomal damages in the normal cells during cancer chemotherapy by adriamycin, and may act as an anticlastogen against induction of micronuclei by superoxide generating agent such as adriamycin.