Genotoxicity of acrylamide and its metabolite glycidamide administered in drinking water to male and female Big Blue mice
Genotoxicity of acrylamide and its metabolite glycidamide administered in drinking water to male and female Big Blue mice
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DOI：
10.1002/em.20157
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发表时间：
2006-01-01
影响因子：
2.8
通讯作者：
Doerge, DR
中科院分区：
文献类型：
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作者：
Manjanatha, MG;Aidoo, A;Doerge, DR
最近在各种油炸和烘焙的淀粉食品中发现了丙烯酰胺(AA)，这是一种可能的人类致癌物质，它的遗传毒性和致癌作用引起了人们的关注。有证据表明，AA的环氧化物代谢物缩水甘草胺(GA)与AA的遗传毒性作用有关。为研究AA的体内遗传毒性，将雄性和雌性大蓝(BB)小鼠按0、100、500 mg/L剂量或等摩尔剂量的GA分别饮水染毒3~4周。在治疗结束后24小时内检测外周血中微核网织红细胞(MN-RET)，并在最后一次治疗21天后进行淋巴细胞HPRT和肝脏CLL突变检测。此外，通过序列分析确定了AA和6 A在肝脏中诱导的CLL突变的类型。大剂量AA和GA处理的男性MN-RETS频率增加1.7-3.3倍(P
The recent discovery of acrylamide (AA), a probable human carcinogen, in a variety of fried and baked starchy foods has drawn attention to its genotoxicity and carcinogenicity. Evidence suggests that glycidamide (GA), the epoxide metabolite of AA, is responsible for the genotoxic effects of AA. To investigate the in vivo genotoxicity of AA, groups of male and female Big Blue (BB) mice were administered 0, 100, or 500 mg/l of AA or equimolar doses of GA, in drinking water, for 3-4 weeks. Micronucleated reticulocytes (MN-RETs) were assessed in peripheral blood within 24 hr of the lost treatment, and lymphocyte Hprt and liver cll mutagenesis assays were conducted 21 days following the last treatment. Further the types of cll mutations induced by AA and 6 A in the liver were determined by sequence analysis. The frequency of MN-RETs was increased 1.7-3.3-fold in males treated with the high doses of AA and GA (P