Cysteine oxidase and cysteine sulfinic acid decarboxylase in developing rat liver

Loriette, C; Chatagner, Fernande

doi:10.1007/bf01915299

Cited by 38 publications

(21 citation statements)

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“…This increase in circulating sulfate level is correlated with increased maternal renal sulfate reabsorption [9,12]. Since the fetus has a relatively low capacity to form sulfate from methionine and cysteine [13,14], most of its sulfate must come from the maternal circulating sulfate pool. These findings are relevant to the decreased fecundity of NaS1 knockout (Nas1 -/-) mice which exhibit both hyposulfataemia and mid-gestational miscarriage [15].…”

mentioning

confidence: 99%

Fetal Loss and Hyposulfataemia in Pregnant NaS1 Transporter Null Mice

Dawson

Sim

Simmons

et al. 2011

Journal of Reproduction and Development

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Abstract. Sulfate is important for growth and development, and is supplied from mother to fetus throughout pregnancy. We used NaS1 sulfate transporter null (Nas1 -/-) mice to investigate the role of NaS1 in maintaining sulfate homeostasis during pregnancy and to determine the physiological consequences of maternal hyposulfataemia on fetal, placental and postnatal growth. We show that maternal serum (≤0.5 mM), fetal serum (<0.1 mM) and amniotic fluid (≤0.5 mM) sulfate levels were significantly lower in pregnant Nas1 -/-mice when compared with maternal serum (≈2.0 mM), fetal serum (≈1.5 mM) and amniotic fluid (≈1.7 mM) sulfate levels in pregnant Nas1 +/+ mice. After 12 days of pregnancy, fetal reabsorptions led to markedly reduced (by ≥50%) fetal numbers in Nas1 -/-mice. Placental labyrinth and spongiotrophoblast layers were increased (by ≈140%) in pregnant Nas1 -/-mice when compared to pregnant Nas1 +/+ mice. Birth weights of progeny from female Nas1 -/-mice were increased (by ≈7%) when compared to progeny of Nas1 +/+ mice. These findings show that NaS1 is essential to maintain high maternal and fetal sulfate levels, which is important for maintaining pregnancy, placental development and normal birth weight. Key words: Placenta, Pregnancy, Sulfate (J. Reprod. Dev. 57: [444][445][446][447][448][449] 2011) ulfate (SO4 2-) is vital for many processes in fetal growth and development, including neurogenesis and steroid metabolism [1][2][3]. The ratio of sulfonated (inactive) to unconjugated (active) steroids has important implications for many of the steroid-responsive events that regulate placental and fetal growth [4]. For example, placental estradiol-3-sulfate is taken up by the fetal brain, where it is desulfonated by steroid sulfatase to estradiol, which acts as a potent stimulator of fetal adrenocorticotropin secretion and the hypothalamus-pituitary-adrenal axis [5]. In addition, sulfonation of structural components, such as heparan sulfate proteoglycans (HSPGs), is essential for the maintenance of normal structure and function of placental and fetal tissues [6]. Together, these findings demonstrate an important role for sulfate in maintaining steroid and glycosaminoglycan homeostasis in the developing fetus. SO4 2-is obtained from the diet and from the intracellular metabolism of methionine and cysteine [6]. Circulating SO4 2-levels are maintained by the NaS1 sulfate transporter which is expressed in the kidney where it mediates sulfate reabsorption [7]. During pregnancy, maternal blood sulfate levels increase by approximately 2-fold which provides an essential supply to the placenta and developing fetus [8][9][10][11]. This increase in circulating sulfate level is correlated with increased maternal renal sulfate reabsorption [9,12]. Since the fetus has a relatively low capacity to form sulfate from methionine and cysteine [13,14], most of its sulfate must come from the maternal circulating sulfate pool. These findings are relevant to the decreased fecundity of NaS1 knockout (Nas1 -/-) mice which exhibit bot...

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confidence: 99%

Fetal Loss and Hyposulfataemia in Pregnant NaS1 Transporter Null Mice

Dawson

Sim

Simmons

et al. 2011

Journal of Reproduction and Development

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“…injection of [35S]taurine (16) and [1-14C]CSA in pregnant mice (unpublished). The activities of cysteine dioxygenase and C SA decarboxylase have been reported to be significantly low in the rat fetal liver (7,10). From these findings, it is conceivable that 14C from [1-14C]cystine and 35S from [35S]cysteine might be transferred to fetus via placenta mostly as cysteine, not in the GSA or taurine form.…”

Section: Discussionmentioning

confidence: 98%

Tissue distribution and metabolism of radioactive sulfur amino acids ((1-41C)cystine, (35S)cysteine) in pregnant mice; A whole-body autoradiography and its biochemical analysis.

Shimono

Shimada

Yamagata

et al. 1989

Acta Histochem. Cytochem

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Tissue distribution and metabolic fate of 14C from [1-14C]cystine and 35S from [35S]cysteine, both precursors of taurine, in various tissues and organs of pregnant mice were studied by whole-body autoradiographic and biochemical analysis.Autoradiography of whole-body cryosection was performed at 30 min, 3 and 6 hr after i.v. injection of radioactive sulfur amino acids ([1-14C]cystine and [35S] cysteine). In the maternal body, the highest optical density (OD) was observed in the pancreas and then the kidney, small and large intestines, stomach, Harderian gland, liver, salivary gland and mammary gland followed.Low ODs were observed in the brain and skeletal muscle. ODs of 14C and 35S in the placenta were relatively high. In the fetus, high ODs of 14C were observed in the lens and 35S in the cartilage and lens.In the biochemical analysis, the mice were decapitated at the same intervals after injection as those for autoradiography and various tissues were removed. These tissues were fractionated into 6% perchloric acid-soluble, -insoluble and lipid fractions. Total radioactivities (cpm/g wet weight) of 14C and 35S were high in the kidney, pancreas, Harderian gland and stomach, and low in the brain, skeletal muscle and fetus. The liver and bile showed high radioactivities in 35S, but low radioactivities in 14C. These data were in good agreement with those of whole-body autoradiographs. The radioactivities incorporated into the acid-insoluble fraction were high in the pancreas, stomach, large intestine and salivary gland, but low in the liver, kidney and skeletal muscle after injection of [1-14C] cystine and [35S]cysteine. The acid-soluble fractions of the liver, kidney, pancreas and small intestine were analyzed by thin-layer chromatography.The radioactive spots for cysteine, cysteine sulfinic acid (CSA) and taurine were detected, but the radioactive level and its change with time in each radioactive spot were different among the organs.

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“…1B). The final CDO1 and CTH gene expression in human and rodent fetal tissues (Gaull et al, 1972;Loriette and Chatagner, 1978;Rakoczy et al, 2015a), suggests that the developing fetus lacks the capacity to generate sulfate and likely explains the late gestational fetal death in Slc13a4 null-mice when placental sulfate supply from mother to fetus is blocked (Rakoczy et al, 2015b).…”

Section: Sulfate Generation Genesmentioning

confidence: 99%

Genetics and pathophysiology of mammalian sulfate biology

Langford

Hurrion

Dawson

2017

Journal of Genetics and Genomics

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Nutrient sulfate is essential for numerous physiological functions in mammalian growth and development. Accordingly, disruptions to any of the molecular processes that maintain the required biological ratio of sulfonated and unconjugated substrates are likely to have detrimental consequences for mammalian physiology. Molecular processes of sulfate biology can be broadly grouped into four categories: firstly, intracellular sulfate levels are maintained by intermediary metabolism and sulfate transporters that mediate the transfer of sulfate across the plasma membrane; secondly, sulfate is converted to 3'-phosphoadenosine 5'-phosphosulfate (PAPS), which is the universal sulfonate donor for all sulfonation reactions; thirdly, sulfotransferases mediate the intracellular sulfonation of endogenous and exogenous substrates; fourthly, sulfate is removed from substrates via sulfatases. From the literature, we curated 91 human genes that encode all known sulfate transporters, enzymes in pathways of sulfate generation, PAPS synthetases and transporters, sulfotransferases and sulfatases, with a focus on genes that are linked to human and animal pathophysiology. The predominant clinical features linked to these genes include neurological dysfunction, skeletal dysplasias, reduced fecundity and reproduction, and cardiovascular pathologies. Collectively, this review provides reference information for genetic investigations of perturbed mammalian sulfate biology.

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Cysteine oxidase and cysteine sulfinic acid decarboxylase in developing rat liver

Cited by 38 publications

References 9 publications

Fetal Loss and Hyposulfataemia in Pregnant NaS1 Transporter Null Mice

Fetal Loss and Hyposulfataemia in Pregnant NaS1 Transporter Null Mice

Tissue distribution and metabolism of radioactive sulfur amino acids ((1-41C)cystine, (35S)cysteine) in pregnant mice; A whole-body autoradiography and its biochemical analysis.

Genetics and pathophysiology of mammalian sulfate biology

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