Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “GANGLIOSIDES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 541 records · Page 30Linked to original sources

Dual inhibitory effect of gangliosides on phospholipase C-promoted fusion of lipidic vesicles.

The effect of a variety of gangliosides has been tested on the phospholipase C-induced fusion of large unilamellar vesicles. Bilayer composition was phosphatidylcholine:phosphatidylethanolamine: cholesterol (2:1:1 mole ratio) plus the appropriate amounts of glycosphingolipids. Enzyme phosphohydrolase activity, vesicle aggregation, mixing of bilayer lipids and mixing of liposomal aqueous contents were separately assayed. Small amounts ( < 1 mol %) of gangliosides in the lipid bilayer produce a significant inhibition of the above processes. The inhibitory effect of gangliosides increases with the size of the oligosaccharide chain in the polar head group. Inhibition depends in a nonlinear manner on the ganglioside proportion, and is complete at approximately 5 mol %. Inhibition is not due to ganglioside-dependent changes in vesicle curvature or size. Ganglioside inhibition of vesicle fusion is due to two different effects: inhibition of phospholipase C activity and stabilization of the lipid lamellar phase. Enzyme inhibition leads to a parallel decrease of vesicle aggregation and lipid mixing rates. Mixing of aqueous contents, though, is depressed beyond the enzyme inhibition levels. This is explained in terms of the fusion pore requiring a local destabilization of the lipid bilayer, the lamellar structure being stabilized by gangliosides. 31P-NMR and DSC experiments confirm the inhibitory effect of gangliosides in various lamellar-to-nonlamellar transitions.

Animals↗

Lipid domains in the membrane: thermotropic properties of sphingomyelin vesicles containing GM1 ganglioside and cholesterol.

The thermotropic behavior of palmitoylsphingomyelin vesicles containing GM1 ganglioside and cholesterol has been investigated by high-sensitivity differential scanning calorimetry. The thermograms exhibited by binary palmitoylsphingomyelin/GM1 mixtures are resolvable into two components. The relative contribution of the minor component, undetectable in the absence of ganglioside, to the total enthalpy and its transition temperature (>40 degrees C) increase with the concentration of the glycolipid embedded in the vesicles. These data suggest the occurrence of lateral phase separation and that more ordered, higher melting GM1 ganglioside-enriched domains are present within the sphingomyelin bilayer. Studies on binary sphingomyelin/cholesterol mixtures confirmed the known tendency of the sterol to decrease the total enthalpy of sphingomyelin, forming cholesterol-enriched domains. The thermograms exhibited by ternary sphingomyelin/ganglioside/cholesterol mixtures in variable proportions (up to 20% molar GM1 or Chol) displayed, on increasing the content of either the sterol or the ganglioside, features addressable to sphingomyelin/cholesterol (peaks centered at temperature </=40 degrees C, decrease of enthalpy) or to sphingomyelin/GM1 mixtures (peaks centered at a temperature >40 degrees C), respectively. This trend was confirmed by deconvolution analysis, showing that the thermograms are resolvable into components addressable to GM1-enriched and to cholesterol-enriched domains. Taken all together, the results show that the architectural features of sphingomyelin bilayers are strongly dependent on the presence of GM1 ganglioside and cholesterol, whose presence is leading to the formation of separate, GM1-enriched and cholesterol-enriched distinct domains. Ganglioside-sphingomyelin and sphingomyelin-cholesterol, together with mutual ganglioside-ganglioside, interactions could contribute to maintain a network of bonds extending to proteins, forming specialized membrane domains, such as caveolae, or others, whose experimental clues are the glycolipid-enriched detergent-insoluble fractions that can be isolated from cell membranes.

Animals↗

Ganglioside patterns in human spinal cord.

OBJECTIVE: To examine the distribution of gangliosides in human cervical and lumbar spinal cord. SETTING: Magdeburg, Germany. METHODS: The ganglioside distribution of human cervical and lumbar spinal cord enlargements from 10 neurological normal patients was analyzed. Gangliosides were isolated from different areas corresponding to the columna anterior, columna lateralis and columna posterior. RESULTS: Ganglioside GfD1b/GD1b and GD3 were the most abundant gangliosides in all examined tissues. The total concentration of sialic acid bound gangliosides GM2 and GM3 was less than 5%. The GD3 fraction constantly consisted of a double band as assessed by TLC after lipid extraction. There were significant differences in the ganglioside distribution when comparing tissue from the columna anterior, columna lateralis and columna posterior of the lumbar enlargement of the spinal cord. CONCLUSION: Differences in the ganglioside composition in human spinal cord regions may reflect the different function of those molecules in the two regions investigated.

Autopsy↗

Shedding of growth-suppressive gangliosides from glomerular mesangial cells undergoing apoptosis.

BACKGROUND: Apoptosis of glomerular mesangial cells is a common feature in several types of glomerular diseases. However, its pathophysiologic significance is not known. We recently identified gangliosides as a major growth-inhibitory substance in the conditioned medium of mesangial cells. In this report, we tested whether biologically distinct forms of cell fate, apoptosis and necrosis, could modulate ganglioside shedding from mesangial cells. METHODS: Mesangial cells were exposed to low (10 to 40 mJ/cm2) and high (400 mJ/cm2) doses of ultraviolet light to induce apoptosis and necrosis, respectively. Conditioned media were collected and examined for its growth-inhibitory activity for mesangial cells. Ganglioside shedding was analyzed using metabolic labeling and thin-layer chromatography (TLC). RESULTS: Shedding of gangliosides as well as growth-inhibitory activity in the conditioned medium predominantly increased when mesangial cells were undergoing apoptosis in contrast to that of viable or necrotic mesangial cells. The inhibitory substance in the conditioned medium from apoptotic mesangial cells completely fulfilled the characteristic criteria of gangliosides. This substance was less than 3 kD and was sensitive to neuraminidase digestion. Shedding of gangliosides from mesangial cells reduced significantly when apoptosis was inhibited by overexpression of antiapoptotic gene, Bcl-XL. In addition, ganglioside shedding also increased when mesangial cells were exposed to other inducers of apoptosis for mesangial cells (i.e., H2O2 and staurosporin). CONCLUSION: These results provide the novel link between masangial cell apoptosis and increased release of gangliosides that potentially suppress mesangial cell proliferation and thus indicate a mechanism for the negative regulation of mesangial cell growth by apoptosis.

Animals↗

Ganglioside inhibition of fibronectin-mediated cell adhesion to collagen.

Fibronectin mediates the adhesion of cells to collagen by first binding to the collagen substrate, followed by attachment of the cells to the fibronectin-collagen complex. Bovine brain gangliosides were found to block fibronectin-mediated cell adhesion to collagen in a concentration-dependent manner. The gangliosides did not block the binding of fibronectin to collagen but did prevent the attachment of the cells to the fibronectin-collagen complex. Of the individual gangliosides tested, GT1 and GD1a were the most effective inhibitors followed by GD1b greater than GM1 greater than GM2; GM3 was not an inhibitor. The inhibition of cell adhesion also was observed with the oligosaccharide portion of the gangliosides, but not with ceramides or with a variety of free sugars or glycosaminoglycans. Mild periodate oxidation of mixed gangliosides or of GD1a modified their sialic acid residues and the oxidized gangliosides were no longer inhibitory; subsequent reduction with NaBH4 did not restore the inhibitory activity of the modified gangliosides. These results suggest that specific gangliosides or related sialic acid-containing glycoconjugates on the cell surface may act as the receptors for fibronectin.

Animals↗

Binding and transport of gangliosides by prosaposin.

Prosaposin, the precursor of saposins A, B, C, and D, which activate lysosomal hydrolysis of sphingolipids, exists in various tissues and body fluids and is especially abundant in the nervous system. Prosaposin and saposins A,B, C, and D formed stable complexes with 13 different gangliosides as measured by an assay using column chromatography. Gangliosides of the gangliotetraose type (a series) were bound with high affinity, whereas b series gangliosides, O-acetylated gangliosides, and gangliosides with shorter carbohydrate chains, were bound with lower affinity. Prosaposin and saposins transferred gangliosides from donor liposomes to erythrocyte ghost membranes. Prosaposin also stimulated ganglioside GM1 beta-galactosidase more than mature saposins. Prosaposin exists as a secretory protein and as an integral membrane protein, and we propose that prosaposin is active as a ganglioside binding and transport protein in vivo.

Biological Transport↗

Degradation of membrane-bound ganglioside GM1. Stimulation by bis(monoacylglycero)phosphate and the activator proteins SAP-B and GM2-AP.

According to our hypothesis (Fürst, W., and Sandhoff, K. (1992) Biochim. Biophys. Acta 1126, 1-16) glycosphingolipids of the plasma membrane are digested after endocytosis as components of intraendosomal and intralysosomal vesicles and membrane structures. The lysosomal degradation of glycosphingolipids with short oligosaccharide chains by acid exohydrolases requires small, non-enzymatic cofactors, called sphingolipid activator proteins (SAPs). A total of five activator proteins have been identified as follows: namely the saposins SAP-A, -B, -C, and -D, which are derived from the single chain SAP-precursor protein (prosaposin), and the GM2 activator protein. A deficiency of prosaposin results in the storage of ceramide and sphingolipids with short oligosaccharide head groups. The loss of the GM2 activator protein blocks the degradation of the ganglioside GM2. The enzymatic hydrolysis of the ganglioside GM1 is catalyzed by beta-galactosidase, a water-soluble acid exohydrolase. The lack of ganglioside GM1 accumulation in patients suffering from either prosaposin or GM2 activator protein deficiency has led to the hypothesis that SAPs are not needed for the hydrolysis of the ganglioside GM1 in vivo. In this study we demonstrate that an activator protein is required for the enzymatic degradation of membrane-bound ganglioside GM1 and that both SAP-B and the GM2 activator protein significantly enhance the degradation of the ganglioside GM1 by acid beta-galactosidase in a liposomal, detergent-free assay system. These findings offer a possible explanation for the observation that no storage of the ganglioside GM1 has been observed in patients with either isolated prosaposin or isolated GM2 activator deficiency. We also demonstrate that anionic phospholipids such as bis(monoacylglycero)phosphate and phosphatidylinositol, which specifically occur in inner membranes of endosomes and in lysosomes, are essential for the activator-stimulated hydrolysis of the ganglioside GM1. Assays utilizing surface plasmon resonance spectroscopy showed that bis(monoacylglycero)phosphate increases the binding of both beta-galactosidase and activator proteins to substrate-carrying membranes.

Animals↗

Developmental changes in localization of the main ganglioside during sea urchin embryogenesis.

Ganglioside M5 (NeuGcalpha2-6Glcbeta1-1'Cer), the main ganglioside in sea urchin and sand dollar eggs, exists mainly in the endoplasmic reticulum and yolk granules in unfertilized eggs. To study the localization of ganglioside M5 after fertilization, early embryos were stained with an anti-ganglioside M5 monoclonal antibody. Using immunofluorescent and immunoelectron microscopy, intense label was observed in the outer surface and cytoplasm of embryos. These results indicate that ganglioside M5 was secreted during embryogenesis and localized in the extracellular matrix (ECM). When living embryos were incubated in sea water containing 7-nitrobenz-2-oxa-1,3-diazole labeled-ganglioside M5 (NBD-M5), the ECM and plasma membrane were strongly stained. Since the localization of NBD-M5 in the ECM was similar to that of extracellular M5, NBD-M5 was likely to be useful to examine the fate of extracellular ganglioside M5. Interestingly, NBD-M5 was incorporated in subcortical vesicles during embryogenesis, suggesting that the extracellular ganglioside M5 is transported into the cytoplasm. When fertilized eggs were incubated with NBD-M5 and tetramethylrhodamine dextran (a marker dye for endocytotic vesicles), colocalization of the dyes was observed in the vesicles. Thus, it was concluded that NBD-M5 in the ECM and/or plasma membrane was internalized in the cells by endocytosis, suggesting that extracellular M5 is transported from the ECM to endocytotic vesicles.

Animals↗

Selective ganglioside desialylation in the plasma membrane of human neuroblastoma cells.

Gangliosides of the plasma membrane are important modulators of cellular functions. Previous work from our laboratory had suggested that a plasma membrane sialidase was involved in growth control and differentiation in cultured human neuroblastoma cells (SK-N-MC), but its substrates had remained obscure. We now performed sialidase specificity studies in subcellular fractions and found ganglioside GM3 desialylating activity in presence of Triton X-100 to be associated with the plasma membrane, but absent in lysosomes. This Triton-activated plasma membrane enzyme desialylated also gangliosides GD1a, GD1b, and GT1b, thereby forming GM1; cleavage of GM1 and GM2, however, was not observed. Sialidase activity towards the glycoprotein fetuin with modified C-7 sialic acids and towards 4-methylumbelliferyl neuraminate was solely found in lysosomal, but not in plasma membrane fractions. The role of the plasma membrane sialidase in gangliosides desialylation of living cells was examined by following the fate of [3H]galactose-labelled individual gangliosides in pulse-chase experiments in absence and presence of the extracellular sialidase inhibitor 2-deoxy-2,3-dehydro-N-acetylneuraminic acid. When the plasma membrane sialidase was inhibited, radioactivity of all gangliosides chased at the same rate. In the absence of inhibitor, GM3, GD1a, GD1b, GD2, GD3 and GT1b were degraded at a considerably faster rate in confluent cultures, whereas the GM1-pool seemed to be filled by the desialylation of higher gangliosides. The results thus suggest that the plasma membrane sialidase causes selective ganglioside desialylation, and that such surface glycolipid modification triggers growth control and differentiation in human neuroblastoma cells.

Carbohydrate Sequence↗

Characterization of ganglioside expression in human melanoma cells: immunological and biochemical analysis.

The expression of N-glycolylneuraminic acid (NeuGc)-containing gangliosides in human melanoma cells grown both in culture and as xenografts in athymic (nu/nu) mice was analyzed extensively with specific mouse monoclonal antibodies (MAbs). Three MAbs (GMR8, GMR14, and GMR3) specific for GM3(NeuGc), GM2(NeuGc), and GD3(NeuGc-NeuGc-), respectively, were used. Significant differences were observed in the ganglioside compositions between the cultured cells in vitro and the tumors grown in vivo. The major difference was that the cells cultured in serum-free medium did not express any NeuGc-containing gangliosides, whereas those grown in nude mice expressed a number of NeuGc-containing gangliosides, namely GM3(NeuGc), GM2(NeuGc), GD3(NeuAc-NeuGc-), GD3(NeuGc-NeuAc-), and GD3(NeuGc-NeuGc-). The structures of these gangliosides were also determined chemically. No activity of CMP-NeuAc hydroxylase was demonstrated either in the melanoma cells cultured in vitro or in those grown in nude mice, suggesting that these cells incorporated NeuGc-containing glycoconjugates from the mouse sera and converted them to other NeuGc-containing gangliosides. The mouse sera contained only GM2(NeuGc), but not the other NeuGc-containing gangliosides or any NeuAc-containing gangliosides.

Animals↗

Characterization of gangliosides from equine kidney and spleen.

Gangliosides were isolated from equine kidney and spleen, and their carbohydrate and lipid moieties were characterized. Among the long-chain bases, considerable proportions of trihydroxy bases (42.3 to 61.2% of the total bases), in which phytosphingosine was predominant were found in all the ganglioside classes. The other major base was sphingosine. Among the constituent fatty acids, long-chain acids (with a carbon number of more than 20), comprised approximately half the total acids, with some alpha-hydroxy and mono-unsaturated acids. By means of sequential hydrolysis with glycosidases coupled with methylation analysis, the following kidney and spleen gangliosides were characterized: hematoside containing both N-acetyl and N-glycolylneuraminic acids; ganglioside GM2 having both types off sialic acid; ganglioside GM1 having mainly N-glycolylneuraminic acid (83 to 86%); ganglioside GD1a having mainly N-glycolylneuraminic acid (71 to 95%). Ganglioside GD3 containing almost exclusively N-glycolylneuraminic acid (93%) was found in the kidney, and ganglioside GD1b having both types of sialic acid in the spleen.

Animals↗

Interspecies comparison of muscle gangliosides by two-dimensional thin-layer chromatography.

Skeletal muscle gangliosides prepared from ten species of animals (human, monkey, bovine, hog, dog, cat, rabbit, guinea pig, mouse, and chicken) were studied by two-dimensional thin-layer chromatography. Densitometric quantification of spots on the chromatograms was carried out with an image analysis system equipped with a computer system. In about thirty-five resorcinol-positive spots, sixteen components could be identified by comparison with authentic standards we had previously obtained. GM3 ganglioside was found as a major component in all examined animals, but there were remarkable species variations in the minor gangliosides. In bovine and hog muscle gangliosides, more than fifteen minor components were detected owing to the presence of N-glycolyl neuraminic acid species. In contrast to this, muscle gangliosides of human, dog, cat, rabbit, and chicken showed relatively simple patterns because of the absence or the small amounts of N-glycolyl type gangliosides. The presence of lactosamine containing gangliosides was characteristic of muscle gangliosides of the examined species.

Animals↗

Growth inhibition of cultured human glioma cells by beta-interferon is not dependent on changes in ganglioside composition.

This investigation tested the hypothesis that the growth inhibiting effects of human beta-interferon on cultured human glioma cells involves changes in the ganglioside composition of these cells. Four cell lines derived from human malignant gliomas (12-18, U-251 MG, I29-A, 7-24) and two lines from human fetal brain (CHI, CHII) were cultured in the presence and in the absence of human beta-interferon (HuIFN-beta), 1,000 units per ml medium for three days before harvesting. Human beta-interferon had an inhibitory effect on growth of glioma but not fetal brain cells. Total ganglioside sialic acid for all cell lines ranged between 3.5 and 13.8 micrograms/10(7) cells (0.6-3.9 micrograms/mg protein). No distinct difference in the amount of total ganglioside per cell was observed between neoplastic and non-neoplastic cells, but the latter had more ganglioside per mg total protein. All cell lines displayed different patterns of gangliosides determined by high performance thin layer chromatography, but there was no distinct difference between glioma and fetal brain cells. Human beta-interferon increased the total amount of ganglioside per cell in one fetal brain and two glioma lines, but on a protein basis in only one glioma cell line (I29-A); HuIFN-beta had only minor effects on ganglioside patterns. There was a slight shift towards a greater proportion of structurally simpler gangliosides in both fetal brain and two glioma cell lines exposed to HuIFN-beta, but the reverse occurred in glioma U-251 MG. None of these changes strongly correlated with the degree of growth inhibition due to HuIFN-beta.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain Neoplasms↗

Pancreatic gangliosides delay the onset of insulitis and hyperglycaemia in the low-dose streptozotocin mouse model.

Gangliosides have been shown to modulate autoimmune phenomena in experimental diabetes. The effects of a pancreatic ganglioside preparation or of a commercial brain ganglioside mixture on the insulitis and blood glucose levels in the low-dose streptozotocin mouse model of diabetes have been investigated. Fifty-five C57BL/6J male mice were grouped as follows: Group 1 (n = 20) was injected intraperitoneally with repeated low doses of streptozotocin; Group 2 (n = 10) received streptozotocin as above but was also injected with a pancreatic ganglioside preparation equivalent to 2 micrograms sialic acid 2 h before each streptozotocin dose; Group 3 (n = 15) received streptozotocin and brain-derived gangliosides in the same dose as that of pancreatic gangliosides; Group 4 (n = 10) consisted of normal animals. Half of the mice were killed on day 12 and the others on day 24 from the beginning of treatment. On day 12, among the streptozotocin-injected animals only those treated with pancreatic gangliosides remained normoglycaemic, whereas on day 24 all streptozotocin mice were hyperglycaemic. Such a result paralleled the data pertaining to insulitis scores. In conclusion, pancreatic gangliosides have a short-term protective role on the development of diabetes in the low-dose streptozotocin model, an effect therefore linked to tissue-related differences in the glycosphingolipid composition.

Animals↗

Gangliosides of calf thymus and of normal and leukemic bovine lymphocytes.

The gangliosides of calf thymus and of lymphocytes from blood, lymph nodes, lymph and spleen of normal and leukemic cows were investigated in an attempt to determine whether there exists a relation between the ganglioside composition and the maturity of the lymphocytes. With all normal peripheral lymphocytes studied the largely prevailing (up to 97%) ganglioside component was found to be N-glycoloylneuraminosyllactosylceramide. The ganglioside spectrum of calf thymus was much more complex and included at least six different components. By thin-layer chromatography, methylation analysis and neuraminidase treatment they were identified as N-glycoloylneuraminosyl and N-acetylneuraminosyl lactosylceramides, N-glycoloylneuraminosylneolactotetraosylceramide, di-(N-glycoloylneuraminosyl), di-(N-acetylneuraminosyl) lactosylceramides and N-glycoloylneuraminosyl-N-acetylneuraminosyllactosylceramide. The ganglioside spectra of leukemic peripheral lymphocytes were different from those of normal peripheral lymphocytes and resembled the ganglioside profile of the thymus. The data obtained indicate that, in the normal animal, the development of thymocytes into mature peripheral lymphocytes is accompanied by loss of disialosyl-gangliosides and sialosylneolactotetraosylceramide. It is concluded that both the structure and the composition of the lymphocyte ganglioside become more simple during maturation and ageing of the lymphocyte.

Animals↗

Gangliosides in normal human serum. Concentration, pattern and transport by lipoproteins.

The total content and pattern of gangliosides were determined in the unfractionated sera of 11 healthy human adults and in isolated lipoproteins. The total content of lipid-bound sialic acid was 10.5 +/- 3.2 nmol/ml serum. The ganglioside profile consisted of more than ten different components. The major ganglioside was GM3, followed by GD3, GD1a, GM2, GT1b, MG-3 (sialosyllactoneotetraosylceramide), GD1b and GQ1b. Traces of four additional gangliosides could not be quantified reliably. Ganglioside patterns did not vary in sera taken from healthy adults of different age and sex. Approximately 98% of human serum gangliosides were transported by serum lipoproteins, predominantly by LDL (66%), followed by HDL (25%) and VLDL (7%). The quantitative distribution of individual gangliosides in VLDL and LDL was almost the same as that in the unfractionated serum; some differences existed with the ganglioside profile in HDL.

Adult↗

Gangliosides of human cerebral astrocytomas.

Ganglioside content and composition were examined in a series of 25 human gliomas, which were graded histologically by the criteria of Kernohan. The concentration of total gangliosides (lipid-bound sialic acid [LBSA]) was decreased with respect to normal brain tissue in nearly all tumors, and the extent of reduction correlated with the stage of tumor anaplasia. The distribution of individual gangliosides was altered in glial tumor tissue with an increase in proportion of the structurally simple gangliosides and reduction of polysialogangliosides. The most consistent and significant difference was the elevation of proportion of ganglioside GD3 from 4-5% of total LBSA in normal brain to 20% in the astrocytoma grade IV. The proportions of gangliosides GM2 and GD2 were also found to be elevated in all grades of the tumors. The simplification of ganglioside composition seems to be associated with transformation of the astrocyte with the accumulation of the simpler gangliosides, since the changes resemble those reported with in vitro transformation rather than those of analyses of preparations of purified glial cells.

Astrocytoma↗

Chloroquine intoxication induces ganglioside storage in nervous tissue: a chemical and histopathological study of brain, spinal cord, dorsal root ganglia, and retinal in the miniature pig.

The effect of chronic chloroquine intoxication on lipid composition, particularly the gangliosides, was studied in the nervous system of miniature pigs, type Göttingen. The tissues examined were cerebrum, spinal cord, dorsal root ganglia and retina. Chloroquine was given in the diet in doses of 2.0-3.5 g/kg good. The intoxication of the pigs was started at the age of 100-240 days and continued for 177-219 days. The control pigs received the same diet without chloroquine. The ganglioside concentration was increased in all the tissues examined. Dorsal root ganglia and retinal were the tissues affected most and showed a twofold increase. This corresponded to the light and electron microscopically demonstrated extensive storage process in the perikarya of dorsal root ganglion cells and inner ganglion cells of the retinal. Under light microscopy the storage material was granular, intensely PAS-positive and dissolved by paraffin embedding. The electron microscopical equivalent consisted of conglomerates of membranous lysosomal residual bodies. In cerebrum the ganglioside concentration was increased by 12%. Storage in the brain varied widely between different systems and types of cells. The allocortex was much more affected than the isocortex. Certain inhibitory ganglion cell types, such as the basket cells, exhibited the most massive storage of all. The spinal medulla was morphologically less involved but showed approximately the same ganglioside increase, though not statistically significant. With the exception of cerebrum the increase in the tissues examined involved all the individual gangliosides, most severely ganglioside GM2 and three fucogangliosides. In cerebrum only the ganglioside GM2 was increased more than the other gangliosides. Chloroquine intoxication did not affect the concentration of phospholipids or cholesterol in the cerebrum, spinal cord or dorsal root ganglia, but in retina the acidic phospholipids were significantly increased.

Animals↗