杂环胺被胰腺组织激活时的致突变性

Terence Lawson, Carol Kolar
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引用次数: 11

摘要

杂环胺(HA) 2-氨基二吡啶[1,2-a:3 ' 2-d]咪唑(Glu-P-2)、2-氨基-3,4-二甲基咪唑- [4,5-f]喹啉(MeIQ)和2-氨基- 1 -甲基-6-苯基咪唑[4,5-b]吡啶(PhIP)对V79细胞(中国鼠肺纤维母细胞)具有致突变性,并以6-硫鸟嘌呤耐药性作为致突变性标志。使用未处理仓鼠的胰管上皮细胞(DEC)、未处理仓鼠的胰管匀浆、高脂饮食仓鼠的胰管匀浆和人DEC来激活杂环胺。当使用仓鼠细胞和组织时,测得的最佳突变频率(突变体/106名幸存者)为:Glu-P-2, 10±1;MeIQ分别为28±2 (DEC)、12±2(对照组,管道匀浆)和21±2(高脂饲料,管道匀浆);PhIP, 61±5。当使用人DEC时,最佳突变频率为:MeIQ, 32±4;PhIP、35±3.3,8-二甲基咪唑[4,5-f]喹诺啉、3-氨基-1,4-二甲基- 5h -吡哆[4,3-b]吲哚和3-氨基-1-甲基- 5h -吡哆[4,3-b]吲哚均无诱变作用
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mutagenicity of heterocyclic amines when activated by pancreas tissue

The heterocyclic amines (HA) 2-aminodipyridol[1,2-a:3′2-d]imidazole (Glu-P-2), 2-amino-3,4-dimethylimidazo- [4,5-f]quinoline (MeIQ) and 2-amino-l-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) were mutagenic in V79 cells (Chinese hamster lung fibrobalsts) using 6-thioguanine resistance as the marker of mutagenicity. Pancreas duct epithelial cells (DEC) from untreated hamsters, homogenates of pancreas ducts from untreated hamsters and those fed a high fat diet and human DEC were used to activate the heterocyclic amines. When hamster cells and tissues were used the optimum mutation frequencies ( mutants/106 survivors) measured were: Glu-P-2, 10±1; MeIQ, 28±2 (DEC), 12±2 (control, duct homogenate, and 21±2 (high fat diet fed, duct homogenate); PhIP, 61±5. When human DEC were used the optimum mutation frequencies were: MeIQ, 32±4; PhIP, 35±3.3,8-Dimethylimidazo[4,5-f]quinoxaline, 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]dole and 3-amino-1-methyl-5H-pyridol[4,3-b]indole were not mutagenic in this assay

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