Sulfate in human pregnancy: what we ought to know. — ASN Events
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Sulfate in human pregnancy: what we ought to know. (#100)

Paul A Dawson 1 2 3 , Joanna Rakoczy 1 2 3 , Scott Petersen 1 4 , Harold D McIntyre 1 4 5 , David G Simmons 3
  1. Mater Research, South Brisbane, Queensland, Australia
  2. Translational Research Institute, Woolloongabba, Queensland, Australia
  3. School of Biomedical Sciences, University of Queensland, St. Lucia, QLD, Australia
  4. Mater Mothers' Hospital, South Brisbane, QLD, Australia
  5. Mater Clinical School, University of Queensland, South Brisbane, QLD, Australia

Sulfate contributes to numerous physiological processes, particularly during pregnancy. Sulfate conjugation (sulfonation) leads to the inactivation of steroids and thyroid hormone, and the detoxification of certain drugs and xenobiotics. In addition, sulfonation of proteoglycans contributes to the normal structure and function of tissues. Importantly, the ratio of sulfonated to unconjugated molecules plays a significant role in many of the molecular events that regulate growth and development.


In humans, the fetus is unable to generate sulfate and therefore relies on sulfate being supplied from the mother. To meet the gestational needs of the fetus, maternal blood sulfate concentrations increase from ≈230uM in non-pregnant women to 465±10uM (n=109) at 12-20 weeks gestation, with levels peaking (506±10, n=109) at 30-37 weeks gestation. These findings are remarkable since most circulating analytes usually decrease slightly due to haemodilution, indicating the importance of high maternal sulfate levels during pregnancy.


The increased sulfataemia during pregnancy is due to enhanced renal reabsorption of sulfate from the maternal urine: fractional excretion index decreases from ≈0.32 in non-pregnant women to 0.16±0.01 (n=109) and 0.13±0.01 (n=109) at 12-20 and 30-37 weeks gestation, respectively. Slc13a1 and Slc26a1 sulfate transporters mediate sulfate reabsorption and we have shown increased (≈2-fold) kidney Slc13a1 and Slc26a1 mRNA levels in pregnant mice. Loss of Slc13a1 and Slc26a1 is linked to renal sulfate wasting, which leads to maternal and fetal sulfate deficiency, and reduced fecundity. Furthermore, loss of the placental Slc13a4 sulfate transporter in mice is linked to perturbed fetal development and late gestational fetal death.


Our studies in mice have prompted us to investigate the consequences of maternal and fetal sulfate deficiency on health outcomes for mother and child. Our studies are also unravelling the sulfate status of preterm babies, which are born at a gestational age when they lack the capacity to generate their own sulfate.

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