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Sulfoglycolipids are an important group of negatively charged biological compounds that have essential and farreaching cellular functions. They are especially active in interacting with extracellular matrix proteins, cellular adhesive receptors, blood coagulation systems, and microorganisms.1 Sulfated glycolipids are produced by action of the enzyme cerebroside sulfotransferase (CST) which transfers a sulfate to the sugar moiety. Sulfated-lactosylceramide was shown to abrogate anchorage-independent growth and cell adhesion to laminin and fibronectin, which could be attributed to decreased β1 integrin gene expression. This led to a novel hypothesis that specific, individual, glycosphingolipids might regulate the gene expression of a select number of genes.2 Sulfated-lactosylceramide binds L-selectin and P-selectin, specific cell adhesion molecules found on cell surfaces and linked to metastasis.3 The presence of sulfated-lactosylceramide was linked to upregulation of CST gene expression and also mediated cell adhesion to vitronectin and αVβ3 integrins. Expression of sulfated-lactosylceramide induced by CST transfection in murine Lewis lung carcinoma cells led to suppression of cell adhesion to laminin and β1 integrin and, subsequently, metastasis.3 Arylsulfatase A is a lysosomal enzyme that catalyzes the first step in the degradation of sulfoglycolipids. Metachromatic leukodystrophy is an autosomal recessively inherited lysosomal storage disorder caused by deficiency of arylsulfatase A activity leading to subsequent accumulation of sulfoglycolipids. Toxic levels of these accumulated lipids leads to ataxia, flaccid and spastic tetraparesis, optical atrophy, epileptic seizures, and other neurological symptoms.4
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