Background: Genistein was reported to adversely influence fetal development although this is yet to be fully understood as a mechanism. Methods: In this study, pregnant rats were divided into control (Cont.) and genistein force-fed (2-mg/kg and 4-mg/kg) groups. Each group was divided further into five subgroups: GD-0, GD-6, GD-13, GD-18, and GD-20 based on the terminal gestational day (GD). On the respective terminal GD, the rats were sacrificed and blood samples and amniotic fluid were carefully collected and separated and placenta homogenates were prepared. These samples were evaluated for oxidative stress and inflammatory reaction. The weights of embryonic implant and placenta tissue were also recorded. Heat shock protein (Hsp) (60 and 90), corticosterone, and oxidative stress biomarkers were determined in all the samples. Results: Fetal and placental weights in all genisteinexposed groups were significantly decreased. A fluctuation in the level of the Hsp was recorded with a significant decrease recorded in Hsp90 level in the placenta and amniotic fluid towards GD-20 along with a concomitant increase in the corticosterone level in the amniotic fluid in all genistein groups compared to control. Maternal serum at GD-18 and GD -20 recorded a significant increase in antioxidant level (SOD, GSH, CAT) in all genisteinexposed groups. However, these antioxidants were significantly reduced in the placenta and the amniotic fluid compared to control. Conclusions: Genistein enhances the placenta function in attenuating the risk of oxidative stress in the amniotic fluid and deferentially suppressed inflammatory activities in the placenta during early gestation and towards late gestation period.