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At least 1,135 records · Page 63Linked to original sources
PubMed1990

Influence of colchicine on the addition of a sugar to the enamel protein in secretory ameloblasts of cultured germs of rat molar tooth by 3H-galactose radioautography.

The influence of colchicine on the addition of 3H-galactose to the enamel protein in secretory ameloblasts of cultured germs of rat molar tooth was investigated by light- and electron-microscopic radioautography. In tooth germs cultured without colchicine, the reaction products of 3H-galactose were observed over Golgi cisternae at early chase times and then localized over the enamel with time. In tooth germs cultured with colchicine, the silver grains were seen over the Golgi cisternae, condensing granules and accumulated secretory granules. Some grains also appeared with time over the pale granular material precipitated in the intercellular space with colchicine treatment. In quantitative analysis with light microscopic radioautography, values of silver grain counts over the unit area (100 microns2) on ameloblasts and enamel of colchicine-treated tooth germs were significantly lower at both 0 min and 30 min chase after 30 min pulse than those of control tooth germs, respectively. This finding indicates that colchicine diminished the incorporation of 3H-galactose into the secretory ameloblast of cultured tooth germs. It is suggested that colchicine decreases the activity of the Golgi apparatus with regard to the addition of sugar to the synthesizing glycoprotein in the secretory ameloblast.

Ameloblasts↗
PubMed1987

Sequence of the mglB gene from Escherichia coli K12: comparison of wild-type and mutant galactose chemoreceptors.

The mglB gene of Escherichia coli codes for a galactose-binding protein (GBP) that serves both as the galactose chemoreceptor and as the recognition component of the beta-methylgalactoside transport system. The mglB551 mutation eliminates the chemotactic function of GBP without altering its transport or substrate-binding properties. To investigate the interaction between GBP and Trg, the chemotactic signal transducer for galactose, we sequenced the mglB genes from wild-type and mglB551 mutant strains. The mutation causes the replacement of Gly74 of GBP by Asp. This residue is located in alpha-Helix III at the tip of the P domain in the GBP tertiary structure farthest removed from the substrate-binding cleft between the P and Q domains. We conclude that Helix III must be part of, or at least adjacent to, the recognition site for Trg. Our sequence also included part of the mglA gene, which is immediately distal to mglB. The amino acid sequence deduced for the beginning of the MglA protein showed homology with a family of polypeptides that contain an ATP-binding site and are components of binding-protein-dependent transport systems.

Amino Acid Sequence↗
PubMed1987

Inhibition of liver metastasis in mice by blocking hepatocyte lectins with arabinogalactan infusions and D-galactose.

According to our hypothesis, organ-specific lectins (e.g., the D-galactose-specific hepatic binding protein) play an important role in the organ location of metastatic malignant cells. The rapid clearance and uptake by the liver of tritiated alpha 1-acid-(asialo)glycoprotein from the circulation of Balb/c mice was markedly delayed after preinjection of D-galactose or arabinogalactan. The preinjection (1 h) and regular application (for 3 days after tumor cell inoculation in Balb/c mice) of the receptor blocking agents D-galactose and arabinogalactan prevented the settling of sarcoma L-1 tumor in the liver completely, but did not influence the settling in the lung. Other galactans, dextrans, and phosphate-buffered saline showed no effect. Therefore, when lectins were blocked with competitive-specific glycoconjugates, colonization was prevented.

Animals↗
PubMed1989

A galactose-dependent cmd1 mutant of Saccharomyces cerevisiae: involvement of calmodulin in nuclear division.

The coding region of a yeast calmodulin gene was fused to a galactose-inducible GAL1 promoter, and a conditional-lethal mutant of Saccharomyces cerevisiae, in which the expression of calmodulin was regulated by galactose, was constructed. The mutant grew normally in galactose medium, but in glucose medium, in which the promoter was repressed, it ceased growing after 12-15 h. The growth arrest was associated with a decrease in intracellular calmodulin levels: after 12 h, no intracellular calmodulin protein was detectable. Analysis of the terminal phenotype showed that when the cell stopped growing, it had a bud, a nucleus after S-phase and a short mitotic spindle. Thus, the defect was mainly in nuclear division. Bud growth was partially inhibited in these cells: 27% of the cells stopped growing with a small bud. Furthermore, calmodulin-deficient cells showed elevated rates of chromosome loss, possibly as the result of a defect in the precise segregation of chromosomes.

Amino Acid Sequence↗
PubMed1981

Interval breath hydrogen test in glucose-galactose malabsorption.

A simple test is described for the diagnosis of monosaccharide malabsorption in infancy caused by a congenital defect of glucose and galactose transport. Increased hydrogen (H2) excretion in expired air after ingestion of sugar was used to diagnose this condition in an infant with severe diarrhoea after breast feeding. Abnormal amounts of H2 were excreted after oral administration of glucose and galactose, but not after fructose. A carbohydrate free diet supplemented with fructose resulted in rapid weight gain and disappearance of diarrhoea. The diagnosis of glucose-galactose malabsorption was confirmed by 14C-glucose transport studies on a jejunal mucosal biopsy specimen. These findings indicate that interval breath H2 estimation in mixed expired air is a non-invasive, reliable procedure for detection of monosaccharide malabsorption in infancy.

Air↗
PubMed1987

Lectinhistochemical demonstration of galactose- and N-acetyl-D-galactosamine residues in cells of the rat anterior pituitary.

Lectins are a useful tool for identification of differently glycosylated hypophyseal hormones, prohormones and glycoconjugates without hormone function. Beta-D-galactose and beta-N-acetyl-D-galactosamine (GalNAc) containing glycoconjugates were identified by light microscopy with biotinylated lectins in immunocytochemically localized cells of the anterior pituitary of the rat. Galactose, histochemically detectable by the peanut lectin (PNA), was found at penultimate position of the carbohydrate chain after removal of sialic acid. Galactose containing cells correspond to gonadotrophs and thyrotrophs located mainly in medioanterior regions of the pituitary. The lectins from the soybean (SBA) and horse gram (DBA) both specific for GalNAc residues, are bound to round and also polygonal cells corresponding again to gonadotrophs and thyrotrophs.

Acetylgalactosamine↗
PubMed1977

A gal region mutant that requires cAMP for growth on galactose in an adenyl cyclase negative (cya delta) background.

Strains of Escherichia coli K12 that contain a deletion of the adenyl cyclase gen (cya delta), required for the synthesis of cyclic adenosine-3';5' monophosphate (cAMP), grow on galactose-containing minimal medium. A mutant was isolated that grows on this medium only if cAMP is added. The mutation (designated galP20) is linked to the gal operon region as determined by both generalized transduction with bacteriophage P1 and specialized transduction with bacteriophage lambda. Studies with galP20 cya delta strains as well as gal delta (deletions of the gal operon) cya delta strains indicate that synthesis of the physiologically important transport mechanism for galactose (galactose permease) requires either cAMP or a function mission from both the galdelta strains and the galP20 strain.

Adenylyl Cyclases↗
PubMed1982

The effect of phentolamine on synaptosomal phosphatidylinositol in experimental galactose toxicity.

Abnormal myo-[2-3H]inositol incorporation into phosphatidylinositol has been found in phentolamine-treated synaptosomes that were isolated from the cerebral hemispheres of galactose toxic rats and incubated with [33P]Pi and myo-[2-3H] inositol. In galactose toxic rats phentolamine-stimulated myo-[2-3H]inositol labeling of phosphatidylinositol was 70% greater than in normal animals. This enhanced labeling of synaptosomal phosphatidylinositol in galactose toxic rats during stimulation with phentolamine is in marked contrast to the depressed myo-inositol labeling of phosphatidylinositol reported with acetylcholine stimulation.

Animals↗
PubMed1982

Changes in [3H]galactose uptake in human colonic mucosa with carcinoma: an ultrastructural study.

As part of our investigation on glycoprotein synthesis in pre-malignant colonic epithelium, changes in the uptake of [3H]galactose were studied at the ultrastructural level. Normal control mucosa from rectal biopsies of patients with no known gastro-intestinal disease and mucosa adjacent to carcinoma ('transitional' mucosa) from specimens resected for colo-rectal cancel were compared. These tissues were incubated in TC 199 medium containing [3H]galactose for various intervals of time and for pulse labelling. Silver grain distribution was statistically analysed. The results showed a reduction in the incorporation of the galactose by 'transitional' mucosa. The uptake by this mucosa was less uniform than normal and showed considerable peaking in the endoplasmic reticulum of the goblet cells and in the Golgi of the absorptive cells, suggesting a blockage or alteration in glycoprotein synthesis. The differences were most marked in the middle crypt (the region of differentiation) and in the upper crypt (the region of maturation).

Colon↗
PubMed1980

A comparison of [3H]galactose and [3H]fucose uptake with the morphological and histochemical changes observed in mucous secretion in chemically induced rat colonic carcinoma.

The alterations in carbohydrate metabolism which occur in the distal colon of rats during carcinogenesis induced by dimethylhydrazine were investigated using [3H]galactose and [3H]fucose as glycoprotein precursors. A statistically significant decrease in [3H]galactose uptake was observed in dysplastic epithelia. These findings are consistent with the alterations in mucin composition with predominance of sialomucins shown in these areas by histochemical methods. Furthermore, changes in the gradient of [3H]galactose incorporation along the crypt epithelium were also found in the histological and histochemically non-involved colonic mucosa of dimethylhydrazine-treated rats, as compared with controls. No significant variations were seen in [3H]fucose incorporation. These results correlate well with our previous histochemical observations and are further evidence of the profound alterations in glycoprotein synthesis affecting the whole colonic mucosa during carcinogenesis.

Animals↗
PubMed1989

Intestinal absorption of D-galactose in the presence of extracts from Phaseolus vulgaris hulls.

The relatively low nutritional value of protein from legume seeds has been attributed to the occurrence of some antinutritional factors and the poor content in sulphur aminoacids, which leads to undesirable physiological and biochemical alterations. However, the intimate nature of these processes remains unclear. In order to evaluate the influence of naturally occurring substances of legume constituents on nutrient utilization, the intestinal absorption of D-galactose in the presence of aqueous or alcoholic extracts, obtained from Phaseolus vulgaris hulls, has been measured by use of the in vivo successive absorption technique. Aqueous extracts inhibited significantly (p less than 0.01) the uptake of D-galactose at different times of exposure, while no changes in sugar transport were observed with the alcoholic solutions. Polyamide treatment (a polyphenolic complexing agent) of the aqueous extracts decreased its ability to inhibit sugar uptake. Kinetic studies showed that the aqueous fractions modify Vmax values for D-galactose absorption and also KT data. This inhibition appeared to be reversible after short periods of exposure, affecting mainly the active component of transport. Therefore, it can be suggested that some substances, contained in aqueous extracts of Phaseolus vulgaris reduce sugar absorption. Furthermore, our studies seem to indicate that polyphenols are, at least partly, involved in this phenomenon.

Animals↗
PubMed1992

The simultaneous exposition of galactose and mannose-specific receptors on rat liver macrophages is developmentally regulated.

We studied the simultaneous binding of galactose and mannose-exposing ligands in sinusoidal rat liver cells during development and aging. The galactose-specific receptors were visualized using 17 nm diameter colloidal gold particles coupled with Lactosylated bovine serum albumine (LacBSA), while mannose-specific receptors were localized by means of 5 nm diameter particles adsorbed with mannan. We observed the presence of four different classes of Kupffer cells in relation to the ligands bound. The percentage of each group of Kupffer cells varied in relation to the age of the subject from which the sample was taken. There were few double-labelled cells in the livers from newborn rats, with numbers increasing with age to adulthood, and decreasing again in the older animals. Cells without labelling were in the majority after birth, but they decreased in number up to adulthood and increased again during subsequent aging. The numbers of single-labelled cells did not change significantly during liver maturation. We hypothesize that the exposition of galactose and mannose-specific receptorial systems is regulated by developmental conditions.

Aging↗
PubMed1982

A geographic approach to senile cataracts: possible links with milk consumption, lactase activity, and galactose metabolism.

Examined in this article is presently available evidence for the hypothesis that some types of senile cataracts may be brought on by decades-long consumption of milk and milk products. The author approaches the question from a background of research in the geography and history of dairying as these relate to present-day differences among the world's peoples in prevalence of primary adult lactose malabsorption, which is based on a deficiency of the enzyme lactase in adulthood. Among peoples who have consumed milk in lactose-rich forms over a long historical period, there seems to have been a mutation for persistence of high lactase activity throughout life (PHLA), which distinguishes them from human populations of nonmilking tradition and from most land mammals. PHLA permits greater intestinal hydrolysis of lactose and absorption of galactose by adults. The mutation for PHLA, however, was not accompanied by a second one raising galactokinase activity to high levels through life. The result may be that adults who consume large quantities of milk, who have high lactase activity, lactose hydrolysis, and galactose absorption, suffer repeated small galactose challenges, accumulation of galactitol in the lens, and a greater likelihood of developing senile cataracts.

Adult↗
PubMed1989

Deficit of uridine diphosphate galactose in galactosaemia.

The levels of uridine diphosphate galactose (UDPGal) and uridine diphosphate glucose (UDPGlc) have been determined in liver autopsy samples, erythrocytes and cultured skin fibroblasts from galactosaemic patients and compared to non-galactosaemic controls. In patients with undetectable erythrocyte galactose-1-phosphate uridyltransferase (transferase) activity, the levels of UDPGal were substantially lower than in controls. In patients with detectable transferase activity, even though in less than 1% of normal values, both UDPGal and UDPGlc levels were in the normal range. Incubation of erythrocytes from both galactosaemic patients and normal individuals with 10 mmol/L uridine increased UDPGal and UDPGlc levels several-fold, both in the presence or absence of galactose in the incubation medium. We hypothesize that a deficit of UDPGal is responsible for the late onset clinical manifestations in galactosaemia which include ovarian failure, speech defect and neurological abnormalities. We suggest that uridine administration may be of therapeutic value in raising the intracellular concentrations of UDPGal. We conclude that the transferase reaction, however small in activity, is essential for optimal UDPGal formation.

Cells, Cultured↗
PubMed1989

Prenatal diagnosis of disorders of galactose metabolism.

Of three clinically significant galactose disorders, there is only a real need and experience of prenatal diagnosis in classical galactosaemia. Prenatal diagnosis for this disorder may be carried out by galactose-1-phosphate uridyl transferase assay in cultured amniotic fluid cells or in chorionic villus biopsies and by galactitol estimation in amniotic fluid supernatant. Although the long-term outcome of patients treated on a galactose-restricted diet is recognized to be unsatisfactory, prenatal diagnosis is only rarely performed with a view to terminating the affected pregnancy.

Female↗
PubMed1990

Results of newborn screening for galactose metabolic disorders.

A screening strategy has been used which uses the Paigen and Beutler methods for the determination of galactose and galactose-1-phosphate. A blood spot test for epimerase has also been developed. In the last 10 years, 265,019 samples from newborns have been tested by these methods. Among the 154 screening positives, we have detected seven cases of epimerase-deficient galactosaemia (Type III), seven cases of Duarte/galactosaemia heterozygotes, 48 cases of other various types of heterozygotes, four cases of persistent hypergalactosaemia, three cases of hepatitis and one case of congenital atresia of the bile duct. These results indicate that our screening system has effectively detected the infants with galactose metabolic disorders.

Carbohydrate Metabolism, Inborn Errors↗
PubMed1995

Study of interaction between calcium and zinc on D-galactose intestinal transport.

Zinc is an essential trace element necessary to life. This metal may exert some of its physiological effects by acting directly on cellular membranes, either by altering permeability or by modulating the activity of membrane-bound enzymes. On the other hand, calcium is an essential element in a wide variety of cellular activities. The aim of the present work was to study a possible interaction between zinc and calcium on intestinal transport of D-galactose in jejunum of rabbit in vitro. In media with Ca2+, when ZnCl2 was present at 0.5 or 1 mM, zinc was found to reduce the D-galactose absorption significantly. In Ca(2+)-free media, where CaCl2 was omitted and replaced isotonically with choline chloride, the sugar transport was not modified by zinc. Verapamil at 10(-6) M (blocking mainly Ca2+ transport) did not modify the inhibitory effect of zinc on D-galactose transport. When 10(-6) M of A 23187 (Ca(2+)-specific ionophore) was added with/without Ca2+ to the media, ZnCl2 produced no change in sugar transport. These results could suggest a possible interaction of calcium and zinc for the same chemical groups of membrane, which could affect the intestinal absorption of sugars.

Animals↗
PubMed2000

Galactose-specific adhesin and cytotoxicity of Entamoeba histolytica.

We examined the molecular mechanisms of the cytotoxicity of Entamoeba histolytica, using the loss of transepithelial electrical resistance (TER) of monolayers of Madin-Darby canine-kidney (MDCK) cells on their incubation with axenic trophozoites of the HM1-IMSS strain. Such loss of TER occurs very early (in 2-5 min) and is caused by the opening of tight junctions and the detachment of cells. We used specific inhibitors for three of the four molecules currently accepted as being responsible for cytotoxicity: galactose-specific adhesin(s), phospholipase A, and cysteine proteinases. We also used inhibitors of calcium channels. Axenic trophozoites of E. histolytica strain HM1-IMSS were preincubated with the different inhibitors for 1 h prior to their coincubation with MDCK-cell monolayers. The only inhibitor that effectively blocked the loss of TER caused by the parasite was galactose. We suggest that in this experimental model, galactose-specific adhesin(s) are essential for amebic cytotoxicity.

Animals↗