首页> 外文期刊>Reproductive toxicology >Sub-chronic sulforaphane exposure in CD-1 pregnant mice enhances maternal NADPH quinone oxidoreductase 1 (NQO1) activity and mRNA expression of NQO1, glutathione S-transferase, and glutamate-cysteine ligase: Potential implications for fetal protection against toxicant exposure
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Sub-chronic sulforaphane exposure in CD-1 pregnant mice enhances maternal NADPH quinone oxidoreductase 1 (NQO1) activity and mRNA expression of NQO1, glutathione S-transferase, and glutamate-cysteine ligase: Potential implications for fetal protection against toxicant exposure

机译:CD-1怀孕小鼠的亚慢性萝卜硫素暴露可增强母体NADPH醌氧化还原酶1(NQO1)活性以及NQO1,谷胱甘肽S-转移酶和谷氨酸半胱氨酸连接酶的mRNA表达:对胎儿预防有毒物质暴露的潜在影响

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The study objective was to determine if maternal administration of sulforaphane (SFN) induced Nrf2-controlled genes. In acute studies, when non-pregnant and pregnant mice were orally exposed to SFN (50 or 100. mg/kg) on gestational day (GD) 14 and euthanized after 2, 6 or 24. h, results demonstrated increased GSTM1, NQO1, HO-1, and Gclc mRNA transcript levels in adult liver, but no change in NQO1 activity. In sub-chronic studies, when non-pregnant and pregnant mice were orally exposed to SFN (65. mg/kg) daily for 30 days and euthanized on GD14, results demonstrated a 2- to 3-fold increase in GSTM1, Gclc and NQO1 transcript levels, and a 2-fold increase in NQO1 activity in adult livers. No effects of maternal treatment on fetal liver gene transcript levels or enzyme activity were observed. Demonstration that SFN induces maternal gene expression and activity supports further investigation of SFN as a preventative agent against transplacental toxicity.
机译:研究目的是确定孕产妇萝卜硫素(SFN)是否能诱导Nrf2控制基因。在急性研究中,当未怀孕和怀孕的小鼠在妊娠第14天(GD)口服SFN(50或100. mg / kg)口服,并在2、6或24 h后安乐死,结果表明GSTM1,NQO1,成年肝脏中的HO-1和Gclc mRNA转录水平,但NQO1活性没有变化。在亚慢性研究中,当未怀孕和怀孕的小鼠每天口服SFN(65. mg / kg)暴露30天并在GD14上安乐死时,结果表明GSTM1,Gclc和NQO1增加了2至3倍转录水平,以及成年肝脏中NQO1活性增加2倍。没有观察到母体治疗对胎儿肝脏基因转录水平或酶活性的影响。 SFN诱导母体基因表达和活性的证明支持SFN作为防止胎盘毒性的预防剂的进一步研究。

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