PLACENTAL COPPER TRANSPORT IN THE RAT - III - INTERACTION BETWEEN COPPER AND IRON IN MATERNAL PROTEIN-DEFICIENCY

Copper (Cu) and iron (Fe) metabolism are linked in the haematopoietic process. There is also considerable evidence of a linkage between prot ein intake and mineral sufficiency. The present study tested the hypot hesis that a low protein diet during the second half of gestation in t he rat alters Cu and Fe transport across the placenta and affects the Cu and Fe status of the fetus. Pregnant rats were fed a normal commerc ial diet the first half of gestation, and then assigned either a 20 pe r cent protein (NP) or a 4 per cent protein diet (LP) during the secon d half of gestation. One day before delivery, rats were anaesthetized, fetuses removed and dam tissues and plasma obtained. Other pregnant r ats were injected i.v. with 2.5 mg/kg Cu acetate and sequential sample s of dam blood, fetal blood and placentae were taken from 0 to 60 min. The LP diet produced generalized maternal hypoproteinaemia, and altho ugh there was no difference in fetal plasma albumin, there was a gener alized fetal hypoproteinaemia as well. Fetal haematocrit (Hct) of the LP litters was lower than that of the NP group, but dam Hct was unchan ged. Dam plasma Fe and Cu showed no differences between diets. Dam liv er Cu was unaltered but liver Fe stores were elevated significantly. B efore and after a Cu bolus, the LP placentae retained Cu to a greater extent than those of the NP placentae. Fetal liver Cu and Fe were elev ated in the LP litters compared to the NP group. In conclusion, the LP diet in the dam during the second half of gestation was associated wi th fetal anaemia, hypoproteinaemia, and increased Cu and Fe accumulati on in fetal liver. The higher concentration of Cu and Fe retained in L P placentae during gestation, and confirmed in the Cu challenge, sugge st that Cu and Fe delivery to the fetus is related to placental concen tration and that maternal protein malnutrition is a regulatory factor in fetal mineral homeostasis. (C) 1998 W. B. Saunders Company Ltd.