The objective of this study was to determine if genistein (GEN) modulation of the immune responses might contribute to the increased host resistances to tumors. A time-course study was performed in adult female B6C3F1 mice that had been exposed to GEN for 1-4 weeks at the dose level of 20 mg/kg by gavage. A significant increase in ex vivo cytotoxic T lymphocyte (CTL) activity was observed in the periods of 2 weeks and 4 weeks. Moreover, increased activities of CTLs were associated with a decrease in the percentage of CD4(+)CD25(+) T cells and an increase in the production of interferon-gamma and activation of STAT1 (signal transducer and activator of transcription 1) and STAT4. Additionally, exposure of mice to GEN increased the activities of in vivo CTLs. An increased activity of natural killer (NK) cells was also observed. Further study in the B16F10 tumor model suggested that GEN-mediated enhancement in host resistance to B16F10 tumor was partially related to its potentiating effect on NK cells. Finally, 7,12-dimethylbenz[a]anthracene (DMBA)-induced tumor model was employed to determine the chemopreventive effect of oral GEN treatment. Mice pretreated with GEN for 2 weeks by gavage, the time when an enhanced CTL activity had been produced, had a decreased susceptibility toward DMBA-mediated carcinogenesis, while treatment with GEN after tumor induction conferred no protection. In conclusion, pretreatment with GEN by gavage could enhance host resistances to the B16F10 tumor and DMBA-induced carcinogenesis, suggesting that GEN modulation of immune response was, at least partially, responsible for the antitumor effect of this compound.

Purpose: Antepartum hemorrhage (APH) in women with placenta previa (PP) has been associated with increased perinatal complications. The present study aims to evaluate the maternal and neonatal outcomes, and risk factors related to this condition. Methods: This retrospective study was conducted in the Obstetrics and Gynecology

The objective of the present study was to determine if exposure to the phytoestrogen genistein (GEN) during immune development had any effects on the production of IgE by adult mice following dermal treatment with trimellitic anhydride (TMA), a respiratory allergen. B6C3F1 mice were exposed to GEN either by feeding at 500 ppm or by gavage (20 mg/kg) for varied periods from gestation day (GD) 14 to postnatal day (PND) 84. In utero exposure to GEN by feeding increased the production of IgE at PND 84 in male mice but not in female mice. In male mice, continuous exposure to GEN postnatally diminished the in utero exposure-induced enhancement in serum total IgE production. However, continuous exposure to GEN from GD 14 to PND 84 was required to increase serum total IgE production in female mice. In utero exposure to GEN by gavage increased the production of IgE at PND 84 in female mice but not in male mice when the mice were maintained on the NIH-07 rodent diet in which a medium level of phytoestrogens was present. The enhancement in IgE production after GEN exposure in females but not in males was associated with decreases in the percentages of CD4(+)CD25(+) T suppressor cells, and increases in the natural killer (NK) cell activity, the basal splenocyte proliferation, the expression of CD86 by B cells, and the production of IL-2 and IL-4. Overall, the results demonstrated that GEN differentially modulated the developing immune system in male and female mice, and that more IgE was produced upon exposure to TMA in the adult.

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