Development of Sulfur Depletion in Pregnant and Fetal Rats: Interaction of Protein Restriction and Indole or Salicylamide Administration

McGarry, Patricia C.; Roe, Daphne A.

doi:10.1093/jn/103.9.1279

Cited by 12 publications

(2 citation statements)

References 20 publications

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“…The nutritional value of sulphate in bolstering the growth of laboratory rodents was first reported almost a century ago [ 28 ]. More recent animal studies have shown that restricting sulphate in both food and water can lead to sulphate deficiency and reduced growth, which can be reversed by sulphate supplementation [ 29 , 30 , 31 , 32 ]. In addition, high dietary sulphate intake and administration of sulphate salts (MgSO 4 , Na 2 SO 4 and ZnSO 4 ) can lead to increased circulating sulphataemia and enhanced sulphonation capacity [ 33 , 34 , 35 , 36 , 37 , 38 , 39 ].…”

Section: Sulphate Is Obtained From the Dietmentioning

confidence: 99%

Sulphate in Pregnancy

2015

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Sulphate is an obligate nutrient for healthy growth and development. Sulphate conjugation (sulphonation) of proteoglycans maintains the structure and function of tissues. Sulphonation also regulates the bioactivity of steroids, thyroid hormone, bile acids, catecholamines and cholecystokinin, and detoxifies certain xenobiotics and pharmacological drugs. In adults and children, sulphate is obtained from the diet and from the intracellular metabolism of sulphur-containing amino acids. Dietary sulphate intake can vary greatly and is dependent on the type of food consumed and source of drinking water. Once ingested, sulphate is absorbed into circulation where its level is maintained at approximately 300 μmol/L, making sulphate the fourth most abundant anion in plasma. In pregnant women, circulating sulphate concentrations increase by twofold with levels peaking in late gestation. This increased sulphataemia, which is mediated by up-regulation of sulphate reabsorption in the maternal kidneys, provides a reservoir of sulphate to meet the gestational needs of the developing foetus. The foetus has negligible capacity to generate sulphate and thereby, is completely reliant on sulphate supply from the maternal circulation. Maternal hyposulphataemia leads to foetal sulphate deficiency and late gestational foetal death in mice. In humans, reduced sulphonation capacity has been linked to skeletal dysplasias, ranging from the mildest form, multiple epiphyseal dysplasia, to achondrogenesis Type IB, which results in severe skeletal underdevelopment and death in utero or shortly after birth. Despite being essential for numerous cellular and metabolic functions, the nutrient sulphate is largely unappreciated in clinical settings. This article will review the physiological roles and regulation of sulphate during pregnancy, with a particular focus on animal models of disturbed sulphate homeostasis and links to human pathophysiology.

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Section: Sulphate Is Obtained From the Dietmentioning

confidence: 99%

Sulphate in Pregnancy

2015

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“…In addition, certain physiological conditions (vitamin D depletion, hypokalaemia, metabolic acidosis) and pharmacological drugs (NSAIDS, glucocorticoids) are known to down-regulate SLC13A1 mRNA and protein expression [ 27 ]. Furthermore, dietary sulfate intake is correlated to circulating sulfate levels in both humans and rodents [ 28 , 29 ]. Collectively, these studies highlight the genetic, physiological and dietary contributions to modulation of circulating sulfate levels, which have potential clinical relevance to fetal growth and development in human gestation.…”

Section: Introductionmentioning

confidence: 99%

Reference intervals for plasma sulfate and urinary sulfate excretion in pregnancy

Dawson

Petersen

Rodwell

et al. 2015

BMC Pregnancy Childbirth

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BackgroundSulfate is important for fetal growth and development. During pregnancy, the fetus relies on sulfate from the maternal circulation. We report reference intervals for maternal plasma sulfate levels and fractional excretion index (FEI) for sulfate in pregnancy, as well as sulfate levels in cord blood from term pregnancies.MethodsPlasma and urine were collected from 103 pregnant women of 10-20 weeks gestation and 106 pregnant women of 30-37 weeks gestation. Venous cord plasma was collected from 80 healthy term babies. Sulfate levels were measured by ion chromatography. Plasma and urinary creatinine levels were used to calculate FEI sulfate in pregnant women. Analyses provide reference intervals, and explored the relationship between maternal sulfate data with several prenatal factors.ResultsMedian maternal plasma sulfate levels were 452 μmol/L and 502 μmol/L at 10-20 and 30-37 weeks gestation, respectively, and inversely correlated with FEI sulfate median values of 0.15 and 0.11. Overall reference intervals were 305-710 and 335-701 μmol/L (2.5th; 97.5th percentile; for 10-20 and 30-37 weeks gestation, respectively) for maternal plasma sulfate, and 0.06-0.31 and 0.05-0.28 for maternal FEI sulfate. Term venous cord plasma sulfate median levels were significantly (p = 0.038) higher in female babies (375 μmol/L) when compared to male babies (342 μmol/L), with an overall reference interval of 175-603 μmol/L.ConclusionsWe provide the first reference intervals for maternal plasma sulfate levels and FEI sulfate, as well as cord plasma sulfate levels. These findings provide reference data for further studies of sulfate levels in both mother and child.Electronic supplementary materialThe online version of this article (doi:10.1186/s12884-015-0526-z) contains supplementary material, which is available to authorized users.

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Effects of salicylamide and protein restriction on the skeletal development of the rat fetus

Knight

Roe

1978

Teratology

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Salicylamide has previously been shown to be teratogenic to the rat. Aims of the present study were to examine separate effects and interactions of salicylamide administration and protein restriction on development of the rat fetus. In experiments using Holtzman rats,the percentage of fetal resorptions was significantly increased by drug treatment and by protein restriction. Malformations were seen in fetuses from dams given the drug from the fifth to eleventh days of gestation; the inicdence of these malformations being independent of the diet. Factors affecting appearance of ossification centers included drug dosage, placental and fetal weight and litter size. Protein restriction had no significant effect on the development of centers of ossification. It is concluded that salicylamide, as well as protein restriction, produces adverse effects on pregnancy outcome in the rat.

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Development of Sulfur Depletion in Pregnant and Fetal Rats: Interaction of Protein Restriction and Indole or Salicylamide Administration

Cited by 12 publications

References 20 publications

Sulphate in Pregnancy

Sulphate in Pregnancy

Reference intervals for plasma sulfate and urinary sulfate excretion in pregnancy

Effects of salicylamide and protein restriction on the skeletal development of the rat fetus

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