26.04.2022, 02:18
All cells require inorganic sulfate for normal function. Sulfate is among the most important macronutrients in cells and is the fourth most abundant anion in human plasma (300 μM). Sulfate is the major sulfur source in many organisms, and because it is a hydrophilic anion that cannot passively cross the lipid bilayer of cell membranes, all cells require a mechanism for sulfate influx and efflux to ensure an optimal supply of sulfate in the body. The class of proteins involved in moving sulfate into or out of cells is called sulfate transporters. And there are various of Sulfate may needed in our life, such as Potassium Sulphate, Magnesium Sulphate, Zinc Sulphate, Ammonium Sulphate, Manganese Sulphate, Ferrous Sulphate, Copper Sulphate, Diammonium Phosphate, Monoammonium Phosphate, Monopotassium Phosphate and so on.
To date, numerous sulfate transporters have been identified in tissues and cells from many origins. These include the renal sulfate transporters NaSi-1 and sat-1, the ubiquitously expressed diastrophic dysplasia sulfate transporter DTDST, the intestinal sulfate transporter DRA that is linked to congenital chloride diarrhea, and the erythrocyte anion exchanger AE1. These transporters have only been isolated in the last 10–15 years, and their physiological roles and contributions to body sulfate homeostasis are just now beginning to be determined. This review focuses on the structural and functional properties of mammalian sulfate transporters and highlights some of regulatory mechanisms that control their expression in vivo, under normal physiological and pathophysiological states.
Sulphate contributes to numerous processes in mammalian physiology, particularly during development. Sulphotransferases mediate the sulphate conjugation (sulphonation) of numerous compounds, including steroids, glycosaminoglycans, proteins, neurotransmitters and xenobiotics, transforming their biological activities. Importantly, the ratio of sulphonated to unconjugated molecules plays a significant physiological role in many of the molecular events that regulate mammalian growth and development.
In humans, the fetus is unable to generate its own sulphate and therefore relies on sulphate being supplied from maternal circulation via the placenta. To meet the gestational needs of the growing fetus, maternal blood sulphate concentrations double from mid-gestation. Maternal hyposulphataemia has been linked to fetal sulphate deficiency and late gestational fetal loss in mice. Disorders of sulphonation have also been linked to a number of developmental disorders in humans, including skeletal dysplasias and premature adrenarche. While recognised as an important nutrient in mammalian physiology, sulphate is largely unappreciated in clinical settings. In part, this may be due to technical challenges in measuring sulphate with standard pathology equipment and hence the limited findings of perturbed sulphate homoeostasis affecting human health.
The sulfate ion in clinical medicine has been regarded as an end metabolite of cysteine and methionine, both sulfur-containing amino acids. Sulfate has been associated with an increase in body acidity and has been shown to lead to a drop in fluid osmolarity of body fluids. Despite the fact that sulfate itself does not possess a catalytic function or a role in human energy metabolism, there is outstanding evidence to suggest that sulfate is not a metabolically inert molecule and that it plays a key function in life.
The Sulfate Ion, Sulfate Formation, and Homeostasis
The sulfate ion is the oxidized form of the 16th element of the Periodic Table, sulfur (S6+), which is surrounded tetrahedrally by four oxygen molecules (O2?) forming the divalent anion SO2?4. In nature, sulfate is an inorganic molecule belonging to the group VI oxyanions, which includes other structurally similar members such as selenate, molybdate, tungstate, and chromate. It is an important anion involved in many physiological processes, having numerous biosynthetic and pharmacological functions. Sulfate is involved in a variety of activation and detoxification processes of many endogenous (including glycosaminoglycans, cerebrosides, steroids, catecholamines) and exogenous (acetaminophen, isoproterenol, ibuprofen, salicylate, α-methyldopa) compounds.
To date, numerous sulfate transporters have been identified in tissues and cells from many origins. These include the renal sulfate transporters NaSi-1 and sat-1, the ubiquitously expressed diastrophic dysplasia sulfate transporter DTDST, the intestinal sulfate transporter DRA that is linked to congenital chloride diarrhea, and the erythrocyte anion exchanger AE1. These transporters have only been isolated in the last 10–15 years, and their physiological roles and contributions to body sulfate homeostasis are just now beginning to be determined. This review focuses on the structural and functional properties of mammalian sulfate transporters and highlights some of regulatory mechanisms that control their expression in vivo, under normal physiological and pathophysiological states.
Sulphate contributes to numerous processes in mammalian physiology, particularly during development. Sulphotransferases mediate the sulphate conjugation (sulphonation) of numerous compounds, including steroids, glycosaminoglycans, proteins, neurotransmitters and xenobiotics, transforming their biological activities. Importantly, the ratio of sulphonated to unconjugated molecules plays a significant physiological role in many of the molecular events that regulate mammalian growth and development.
In humans, the fetus is unable to generate its own sulphate and therefore relies on sulphate being supplied from maternal circulation via the placenta. To meet the gestational needs of the growing fetus, maternal blood sulphate concentrations double from mid-gestation. Maternal hyposulphataemia has been linked to fetal sulphate deficiency and late gestational fetal loss in mice. Disorders of sulphonation have also been linked to a number of developmental disorders in humans, including skeletal dysplasias and premature adrenarche. While recognised as an important nutrient in mammalian physiology, sulphate is largely unappreciated in clinical settings. In part, this may be due to technical challenges in measuring sulphate with standard pathology equipment and hence the limited findings of perturbed sulphate homoeostasis affecting human health.
The sulfate ion in clinical medicine has been regarded as an end metabolite of cysteine and methionine, both sulfur-containing amino acids. Sulfate has been associated with an increase in body acidity and has been shown to lead to a drop in fluid osmolarity of body fluids. Despite the fact that sulfate itself does not possess a catalytic function or a role in human energy metabolism, there is outstanding evidence to suggest that sulfate is not a metabolically inert molecule and that it plays a key function in life.
The Sulfate Ion, Sulfate Formation, and Homeostasis
The sulfate ion is the oxidized form of the 16th element of the Periodic Table, sulfur (S6+), which is surrounded tetrahedrally by four oxygen molecules (O2?) forming the divalent anion SO2?4. In nature, sulfate is an inorganic molecule belonging to the group VI oxyanions, which includes other structurally similar members such as selenate, molybdate, tungstate, and chromate. It is an important anion involved in many physiological processes, having numerous biosynthetic and pharmacological functions. Sulfate is involved in a variety of activation and detoxification processes of many endogenous (including glycosaminoglycans, cerebrosides, steroids, catecholamines) and exogenous (acetaminophen, isoproterenol, ibuprofen, salicylate, α-methyldopa) compounds.