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 aga

•Acute exposure to SFN in pregnant mice increased liver GSTM1 and NQO1 mRNA levels.•Acute exposure to SFN in pregnant mice did not increase adult liver NQO1 activity.•Sub-chronic exposure to SFN increased GSTM1 and NQO1 mRNA levels.•Sub-chronic exposure to SFN increased NQO1 activity in adult livers.•Treatment with SFN may protect the fetus against exposure to various toxicants.

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.