Sulfatases

The first step in the complete biodegradation of primary alcohol sulfates seems to be the hydrolysis to yield alcohol. Sulfatases are able to hydrolyze primary alcohol sulfates. Different authors have isolated and used several sulfia-tase enzymes belonging to Pseudomonas species. The alcohol obtained as a result of the hydrolysis, provided that dehydrogenases have been removed to avoid the oxidation of the alcohol, was identified by chromatography and other methods [388-394]. The absence of oxygen uptake in the splitting of different primary alcohol sulfates also confirms the hydrolysis instead of oxidation [395, 396]. The hydrolysis may acidify the medium and stop the bacterial growth in the absence of pH control [397-399]. 

Multiple sul tase deficiency tesults in accumulation of sulfogalactosylcetamide, stetoid sulfates, and proteoglycans owing to a combined deficiency of atyl-sulfatases A, B, and C and stetoid sulfatase. 

Hurler-Scheie (MIM 252800) Hunter (MIM 309900) MPS II Iduronate sulfatase Dermatan sulfate, heparan sulfate... 

Sanfilippo A MPS IIIA Heparan sulfate N-sulfatase Heparan sulfate... 

MIM 252940) Morquio A MPS IVA 6-sulfatase Galactosamine 6-sulfatase Keratan sulfate, chondroitin 6-sulfate... 

MIM 253200) Sly (MIM 253220) MPS VII sulfatase (arylsulfatase B) P-Glucuronidase Dermatan sulfate, heparan sulfate, chondroitin... 

WONG c K, KEUNG w M (1997) Daidzein sulfoconjugates are potent inhibitors of sterol sulfatase (EC 3.1.6.2). Biochem Biophys Res Commun. 233 579-83. 

Arylsulfatase from Pmudamonas aarugmasa Sulfatase from Rhodopimllula baMce ... 

Sulfatase alkylsulfatase from Rhodococcus ruter DSM 44541 E = 21 with additives E = 200 ... 

Although sulfate is formed by hydrolysis of both alkyl and aryl sulfates, the pathway of degradation for aryl sulfates is controlled by the source of sulfur (Cook et al. 1999). The complex issues surrounding the hydrolysis of sulfate esters have been discussed (Kertesz 1999), and are illustrated by the number and substrate specificity of alkyl sulfatases for the surfactant 2-butyloctyl sulfate in Pseudomonas sp. strain AE-A (Ellis et al. 2002). 

Recksiek M, T Selmer, T Dierks, B Schmidt, K von Figura (1998) Sulfatases, trapping of the sulfonated enzyme intermediate by substituting the active site formylglycine. J Biol Chem 273 6096-6103. 

Although hydrolysis of alkyl sulfates by sulfatases is noted in Part 1 of this chapter, ether cleavage has been shown to be the major pathway for the degradation of dodecyltriethoxy sulfate (Hales et al. 1986). 

Based on the data from animal studies, diisopropyl methylphosphonate is principally excreted in the urine as the metabolite IMPA (Hart 1976 Ivie 1980). Chromatographic behavior of urinary metabolites does not change after the urine is treated with glucuronidase and sulfatase, so there is no conjugation of diisopropyl methylphosphonate or IMPA by microsomal enzymes (Hart 1976). There was minimal excretion of diisopropyl methylphosphonate metabolites in bile (Hart 1976) or in the milk of a lactating cow (<1%) (Palmer et al. 1979). 

Sulfatase Cleavage of O-sulfates and sulfamates Cydamate, amygdalin, estrone sulfate... 

The final step is a hydrolyzing step with sulfatase enzymes (E.C. number 3.1.6.1), such as limpet sulfatase, Aerobacter aerogenes sulfatase, Abalone entrail sulfatase, or Helixpomatia sulfatase. This step was suggested to be carried out in a CSTR or fluidized bed reactors, with counter-current flow between the aqueous and the oil phase. A more efficient removal of the sulfate into the aqueous stream is expected to occur in this cross-flow manner. A final separation of the reacting mixture was suggested to obtain sulfur-free product and aqueous enzyme solution for recycle. 

Metachromatic leukodystrophy AR Aryl sulfatase A Accumulation of sulfatide in brain see text 1,2, Ch. 40... 

Hunter s syndrome MPS 11 Iduronate sulfatase Dermatan sulfate Heparan sulfate... 

Maroteaux-Lamy MPS VI AT-acetyl-galactosamine-4-sulfatase Dermatan sulfate... 

Multiple sulfatase deficiency (MSD). The clinical presentation of MSD includes features of MLD and the MPS, with the features that resemble MLD, such as gait disturbances, psychomotor retardation and polyneuropathy predominating. MPS-like features, such as facial coarsening, hepatosplenomegaly and joint stiffness, are present to a milder and variable extent. A reduction in the activity of all sulfatases is the key diagnostic abnormality. Von Figura and associates have demonstrated that catalytic activity of all sulfatases requires a post-translational modification in which a cysteine residue (cysteine 69 in arylsulfatase A) is oxidized to an aldehyde. It is this modification that is defective in MSD [5]. 

Dierks, T., Schmidt, B., Borissenko, L. V. et al. Multiple sulfatase deficiency is caused by mutations in the gene encoding the human Ca-formylglycine generating enzyme. Cell 113 435-444, 2003. 

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