Changes in iron concentrations in fetal mice and expression of iron transport proteins in the placenta during pregnancy as a result of infection with Toxoplasma gondii.

Objective To study the changes in iron concentrations in fetal mice and expression of iron transport proteins in the placenta during pregnancy as a result of infection with Toxoplasma gondii.Methods Experimental models were created by intraperitoneal injection of tachyzoites of T.gondii on the 8th day of pregnancy.The concentration of Fe in fetal mice was determined by flame atomic absorption spectrometry(FAAS).Iron in fetal mice was stained by DAB-enhanced Perls' staining.The expression of ferrportin1(FP1) and ceruloplasmin(Cp) in the placenta was detected immunohistochemically.Results On the 10th day of pregnancy,there was no significant difference in the Fe concentration in fetal mice for the two groups,but the Fe concentration in the experimental group was significantly lower than that in the control group on the 12-18th day of pregnancy(P0.05).Iron staining of the entire fetal mouse and liver and brain of fetal mice in the infected group was significant weaker than that in the control group.FP1 and Cp were expressed in the basal(fetal facing) membrane of the placental syncytiotrophoblast(STB),consistent with unidirectional iron transport from the mother to the fetus.On the 10th and 12th day of pregnancy,there were no significant differences in the expression of FP1 and Cp in the placenta for the two groups(P0.05).However,the expression of FP1 and Cp in the placenta of the experimental group was significantly higher than that in the control group on the 14-18th day of pregnancy(P0.05).Conclusion Infection with T.gondii during pregnancy induced a decrease in the fetal iron concentration,and this phenomenon might be involved in the retardation of fetus growth.The increased expression of FP1 and Cp in the placenta may be the result of compensating for decreased fetal iron.This is indirect evidence that the expression of FP1 and Cp in the placenta might be regulated by fetal iron concentration.