• Title/Summary/Keyword: N-nitro-N-nitrosourea(MNU)

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Antigenotoxicity of Galangin and its Action Mechanism (Galangin의 유전독성 억제효과와 작용기전)

  • 허문영;류재천
    • Environmental Mutagens and Carcinogens
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    • v.18 no.2
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    • pp.77-82
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    • 1998
  • In order to compare the suppressive effect of galangin on the genotoxicity by N-methyl-N-nitrosourea (MNU) or benzo[a]pyrene B(a)P, in vivo micronycleus test using mouse peripheral blood and in vitro sister chromatid exchange(SCE) test using mouse spleen lymphocytes were performed. MNU or B(a)P-induced micronucleated reticulocytes in vivo was decreased by the simultaneous treatment of galangin. MNU or B(a)P-induced SCEs in vitro was also decreased by the simultaneous treatment of galangin. On the other hand, the determinations of [$^3$H]MNU-induced total DNA binding and methylated DNA were performed to find out the mechanism of action. [$^3$H]MNU-induced total DNA binding was inhibited by the treatment of galangin in calf thymus DNA. HPLC analysis of DNA hydrolysates showed that galangin caused a decrease of 7-methyl guanine and $O^{6}$-methyl guanine in calf thymus DNA. To elucidate the action mechanism of galangin against B(a)P, alteration of B(a)P metabolism was studied. Galangin inhibited B(a)P metabolism in the presence of S-9 mix and decreased B(a)P-DNA binding in calf thymus DNA with S-9 mix.

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Antigenotoxicity of Ginseng Petroleum Ether Extract and its Action Mechanism (인삼 지용성성분인 유전독성억제효과와 작용기전)

  • 허문영
    • Journal of Food Hygiene and Safety
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    • v.13 no.3
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    • pp.243-251
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    • 1998
  • Panax ginseng C.A. Meyer has been extensively used in the traditional oriental medicine as a restorative, tonic and prophylatic agent. Petroleum ether extract of panax ginseng C.A. Meyer (GPE) and its several fractions (PI-P5) were tested for the evaluation of antigenotoxicity against N-methyl-N-nitrosourea (MNU) and benzo(a)pyrene [B(a)P]-induced micronucleated reticulocytes in mouse peripheral blood. GPE and P2 showed more significant anticlastogenicity than other fractions did. To elucidate the anticlastogenic action mechanism of GPE and P2 against B(a)P, the alteration of B(a)P metabolism was studied. GPE and P2 inhibited B(a)P metabolism in the presence of 8-9 mix and decreased B(a)P-DNA binding in calf thymus DNA with 8-9 mix. They also decreased [$^3H$] MNU induced DNA binding and methylation to 7-methyl guanine and $O^{6}-methyl$ guanine adducts in calf thymus DNA by RPLC analysis. These results suggest that the anticlastogenicity of GPE and P2 on the B(a)P or MNU-induced clastogenicity is due to decrease of DNA binding with B(a)P or MNU, the inhibition of metabolism with B(a)P and the inhibition of methylation in DNA. Therefore, GPE and P2 may be useful chemopreventive agents of alkylating agent like MNU and secondary carcinogen like B(a)P.

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Regulatory Expression of DNA Repair Genes Involved in Adaptive Response (적응반응 관련 DNA 회복유전자의 발현조절에 관한 연구)

  • 최수영;이희원;박상대
    • Environmental Mutagens and Carcinogens
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    • v.10 no.1
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    • pp.1-10
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    • 1990
  • The regulation of DNA repair genes expression was investigated using fused genes, in which the promoter of repair genes was hybridized with the lacZ structural gene. The activities of beta-galactosidase expressed from the fused gense were highly increased when the host cells were exposed to methylating agents, such as methyl methansulfonate (MMS), N-methyl-N'-nitro-nitrosoguanidine (MNNG) and methyl nitrosourea (MNU). On the other hand, the enzyme activities from the fused genes were not induced when the cells were treated with ethylating or nonalkylating agents, such as ethyl methansulfonate (EMS), 4-nitroquinoline-1-oxide (4NQO), Bleomycin, and Benzo(a)pyrene (BP).

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