Sulfatide appearance

A dramatic increase (approx. 50-fold) of the activity of the sulfotransferase involved in the biosynthesis of the SGG also occurred when spermatocytes first began to appear in rat testis (19) the rise in the activity of this enzyme preceded by several days a marked rise in the amount of the SGG. Studies on pre-puber-tal human testis (which is temporarily blocked in spermatogenesis at a stage prior to the appearance of primary spermatocytes) have shown that neither SGG nor GG is present (15,26). Similarly, the testis of the pre-pubertal fowl also lacks sulfogalactosylceramide, the sulfatide found in mature fowl testis (26). All of these find-... 

Estimates of the rate of myelin synthesis can be obtained in vitro from the measurement of cerebroside synthesis, which increases fourfold from day 10 to day 20 in the rat and then slowly decreases along with the overall rate of myelin synthesis. In vivo studies employing radiolabeled precursors of specific myelin components, such as sulfate into sulfatide, yield results similar to those obtained in vitro. In situ studies with tissue slices confirm in vitro and in vivo experiments. These studies also indicate that the appearance of... 

Little is known of the biosynthesis, breakdown, or role of sulfatides. Two observations seem established the biosynthesis of sulfatides coincides with the appearance of myelin and studies with the aid of a radioactive precursor have established a slow but definite turnover of sulfatides in the adult brain. Consequently, the brain constantly synthesizes and degrades sulfatides. Similar anabolic and catabolic processes are likely to occur in other tissues. 

Cerebrosides and sphingomyelin are believed to accumulate in the globoid bodies. In fact, the injection of cerebrosides into rats has led to the appearance in the white matter of cells that resemble globoid cells. The biochemical defect in Krabbe s disease is still unknown, but two clues are available. There are no defects in sphingomyelin breakdown, there is a shift in the ratio of cerebrosides to sulfatides (from 3 to 1 in the normal individuals to 12 to 1 in those with leukodystrophy. These observations have led to the suggestion [127-130] that the lipidosis results from a deficiency of a sulfate-transferring enzyme (see Fig. 3-43). 

Glycolipids (cerebrosides, sulfatides, gangliosides, and others) appear as yellow spots cholesterol appears as a light red-spot. 

Since the carbohydrate moiety of the monohexose-sulfatide is galactose, as in normals, it appears certain that the stored sulfatide in ML is identical with the normal sulfatide. 

Sulfatides are derived from GalCer via esterification of a sulfate group to 3-hydroxyl of the galactose moiety. Sulfatides are abundant in the brain, where they act as essential components of the myelin sheaths, and also appear to participate... 

A more detailed publication has appeared recently in which sulfatide biosynthesis is described (Cumar et al., 1968). Sulfotransferase activity for ceramide galactoside was detected in all cerebral subceliular particles examined, including the soluble fraction. The bulk of activity was present in the crude mitochondrial portion, presumably in the synaptosomes. ilicrosomes exhibited the highest specific activity and a deoxycholate extract of these particles was examined more extensively. This prepara tion was employed principally for comparison of the sulfation of lactose and ceramide iactoside. An apparent K for ceramide galactoside varying from 3.3 to 8.5 X 10 M was reported. The product had chrnmatr raphic properties similar to sulfatide. 

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