Proceedings of The Physiological Society

Kings College London (2005) J Physiol 565P, C180

Communications

Effect of iron deficiency on embryonic development in the rat.

Andersen, Henriette Skovgaard; Gambling, Lorraine ; Harrison, Susan ; McArdle, Harry John;

1. Development, Growth and Function, Rowett Research Institute, Bucksburn, Aberdeen, United Kingdom.


Iron (Fe) deficiency during pregnancy has serious consequences for both the mother and her offspring leading to perturbed fetal development, abnormal heart development and raised blood pressure in adult life. However, less is known about which developmental stage the embryo is most sensitive to Fe status. To examine this we used an in vitro whole rat embryo culture model. Whole embryo culture involves the culture of gestation day 9 to 11 rat embryos for up to 72 h. This stage corresponds to a period of major organogenesis, making the model ideal for studying mammalian embryonic development. In this study, female Rowett Hooded Listers rats were weaned onto control diet (100% Fe, 50 mg Fe/kg diet) for four weeks then fed either a control or Fe-deficient diet (15% Fe, 7.5 mg Fe/kg diet) for additional four weeks before being mated. The uterine horns were removed by hysterectomy under iso-flourane induced terminal anaesthesia and placed in Tyrodes salt solution. The embryos were dissected free of uterine wall, deciduas and Reicherts membrane and cultured for 48 h in 95 % rat serum collected from male rats fed either a control or a Fe deficient diet. After 48 h yolk sacs and embryos were examined for morphological abnormalities. All experimental procedures were approved and conducted in accordance with the U.K Animals (Scientific Procedures) Act of 1986. Mann Whitney T-test was used to determine statistical significance (p<0.05) between the two groups. Compared to control embryos, the yolk sac diameter of embryos cultured under Fe-deficient (Fe-def) conditions was significantly reduced (Control=4.94 mm + 0.40; Fe-def= 4.59 mm + 0.44; p=0.0013) and the circulation impaired (Control=3.89 + 0.48; Fe-def=3.54 + 0.75, p=0.0493). They were growth retarded having reduced crown-rump length (Control= 4.45 mm + 0.34; Fe-def= 4.16 mm + 0.42, p=0.0062) and fewer somites that the control embryos (Control=32.8 + 0.75; Fe-def= 32.0 + 1.64; p=0.0204). Although growth retarded, the Fe-deficient embryos had significant larger hearts than the control embryos (Control= 62962 + 13618 pixels; Fe-def= 71695 + 15933 pixels; p= 0.041). All data are presented as mean + SD. Minimum of 25 embryos for each group was used for all analyses. In this study it was found that Fe-deficiency caused morphological changes in yolk sac vascularisation, fetal growth retardation and enlargement of the heart. These data indicate an important role of Fe status for yolk sac vascularisation. It is possible that the changes observed in yolk sac morphology might impinge on heart development and affect blood pressure in adult life

Where applicable, experiments conform with Society ethical requirements