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.