Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.23 (beta-galactosidase)
 14,648 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of Fusarium sporotrichiella v. sporotrichioides mycotoxin (sporofusarin) on the total and non-sedimentary supernatant activity of 13 marker-enzymes of subcellular particles (2 mitochondrial enzymes-cytochrome oxidase and malate dehydrogenase; 8 lysosomal enzymes -- acid phosphatase, acid RNAase, acid DNAase, arylsulphatases A and B, beta-N-acetylglucosaminidase, beta-glucuronidase, beta-galactosidase and beta-glucosidase; 2 microsomal enzymes -- glucose-6-phosphatase and acetylesterase; plasma membrane enzyme -- alkaline phosphatase) of the rat liver, kidney, spleen and bone-marrow was studied in in vivo experiments. The latter demonstrated that sporofusarin effects were characterized by a significant organ and organella specificity, viz. the toxin caused a sharply increased activity, mainly of lysosomes enzymes and labilization of the lysosomal membranes, primarily in the spleen and the bone-marrow. A conclusion is drawn that the discovered selective destructive action of sporofusarin on the lysosomes may be regarded as a new phenomenon that, possibly is directly related to the characterization of the mechanism responsible for a specific effect produced by sporofusarin.
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PMID:[Lysosomal component in the mechanism of the toxic effect of sporofusarin]. 94 27

The mannitol influence on mutagenesis of ionizing radiation and cyclophosphate has been studied in albino mongrel rats using the methods of genetic and biochemical analysis. N correlation is determined between antimutagenic action of this preparation and a decrease of malondialdehyde content in cells and free fractions of matrix lysosomes (beta-galactosidase; N-acetyl-beta-D-glucosaminidase) and firmly membrane-structurized microsomal (glucose-6-phosphatase) enzymes, whose level increases under the influence of mutagens. It is shown that, one of the way of antimutagenic actions of mannitol is connected with mutagenesis correction at the stage of origin of mutagenic products and their transport to chromosome DNA.
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PMID:[The interrelation of the antimutagenic action of mannitol to its effect on cellular metabolic processes]. 129 65

We have developed a ligand-specific method for the visualization, isolation, and biochemical characterization of cell surface and intracellular membranes mediating endocytic transport. Iron dextran particles (FeDex) bearing either covalently conjugated galactosyl bovine serum albumin (GalBSA/FeDex) or asialofetuin (ASF/FeDex) are bound by the asialoglycoprotein receptor (ASGP-R) of HepG2 cells and transported to lysosomes with kinetics indistinguishable from those of free GalBSA or ASF. FeDex particles, which have a 3 to 5 nm electron-dense colloidal iron core, can be visualized by electron microscopy. Following incubation of GalBSA/FeDex with HepG2 cells at 37 degrees C, FeDex particles are seen at the cell surface, in endosomes, and in lysosomes. Surface membrane and intracellular organelles bearing a sufficient number of FeDex particles can be efficiently isolated from disrupted cells by high gradient magnetic affinity chromatography (HIMAC). Plasma membranes and endosomal/lysosomal membranes isolated by HIMAC are 35 to 40-fold enriched for GalBSA/FeDex or ASF/FeDex relative to the postnuclear supernatant. Alkaline phosphodiesterase I (APDE) and galactosyltransferase are each enriched 8-fold in the plasma membrane fraction prepared by HIMAC whereas neither beta-galactosidase nor glucose-6-phosphatase are detected in this fraction. The intracellular membrane fraction, containing both endosomes and lysosomes, is enriched for galactosyltransferase and beta-galactosidase but not for APDE or glucose-6-phosphatase. Use of FeDex conjugates in conjunction with HIMAC provides an effective method for ligand-specific isolation of membranes and correlation of morphological and biochemical characteristics.
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PMID:Ligand-specific isolation of endosomes and lysosomes using superparamagnetic colloidal iron dextran glycoconjugates and high gradient magnetic affinity chromatography. 168 Jun 81

Groups of male and groups of female Wistar albino rats were administered diets containing sufficient di(2-ethylhexyl) phthalate (DEHP) to ensure intakes of either 1000, 200, or 50 mg/kg/day. Four rats from each experimental group and six control rats of the same sex were killed 3, 7, 14, and 28 days and 9 months after commencement of treatment. At all time points the major abdominal organs were removed and subjected to histological examination. A more extensive necropsy was performed on those rats killed after 9 months of treatment. At all time points the livers of the rats were subjected to extensive histologic, electron microscopic, and biochemical examination. Changes could be grouped according to their time course. Two early and transient alterations were noticed. First, there were morphologic changes in the bile canaliculi of male rats treated with 1000 mg/kg/day of DEHP. Second, there was a burst of mitosis immediately after the start of administration of the compound. The time course of this mitotic burst varied; the increase in mitosis was greatest at 3 days in rats treated with 1000 mg/kg/day of DEHP and was smaller but more prolonged in rats treated with 200 or 50 mg/kg/day. Other changes, namely, a midzonal to periportal accumulation of fat, induction of peroxisomal enzymes, and induction of the P-450 isoenzyme also developed rapidly but were sustained throughout the study. The maximal change was usually attained within 7 days of commencement of treatment. More slowly developing changes were hypertrophy of the hepatocytes, centrilobular loss of glycogen, and a fall in glucose-6-phosphatase activity. Here maximal changes were not attained until 28 days after commencement of treatment. These three effects were clearly observed in rats treated with 200 or 1000 mg/kg/day of DEHP but were only marginally altered in rats treated with 50 mg/kg/day. Finally accumulation of lipid-loaded lysosomes assessed by light and electron microscopy and by assay of beta-galactosidase activity was only apparent in rats treated with DEHP for 9 months with 200 or 1000 mg/kg/day of DEHP. Changes in female rats were qualitatively similar to those observed in male rats. The alterations were, however, less pronounced than in male rats treated with an equal dose of DEHP and the degree of liver enlargement was much less because, although the initial hyperplasia was clearly apparent, there was a much smaller degree of hypertrophy.
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PMID:Time and dose-response study of the effects on rats of the plasticizer di(2-ethylhexyl) phthalate. 286 21

Subacute experiments were made to examine the effect of the grain contaminated with Fusarium sporotrichiella on the activity of organelle-specific enzymes of the liver, thymus, spleen, bone marrow and blood serum of rats (beta-N-acetylglucosaminidase, alpha-mannosidase, beta-galactosidase, arylsulfatases A and B, succinate dehydrogenase, glucose-6-phosphatase, alkaline phosphatase, ketoso-1-phosphate aldolase) and on the protein content. The feeding of the grain provoked an early appearance of the symptoms of intoxication and a change in the activity of organelle-specific enzymes manifesting in the activation of lysosomal hydrolases in the thymus, bone marrow and spleen and in a decrease in the blood serum activity of the most enzymes investigated.
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PMID:[Enzyme characteristics of food poisoning caused by grain contaminated with Fusarium sporotrichiella]. 642 31

The pregnant rats were treated with formaldehyde (0.5 mg/kg daily per os) during whole period of pregnancy. The activity of cytochrome-c-oxidase, malate dehydrogenase, nucleotidase, glucose-6-phosphatase, beta-glucuronidase, N-acetyl-beta-glucosaminidase, beta-galactosidase, H(+)-ATPase, glutamate dehydrogenase, NAD- and NADP-isocitrate dehydrogenase, fructose-bisphosphate aldolase, glucose-6-phosphate dehydrogenase and content of protein in liver celts of offsprings (newborns, 2 weeks age and 2 months age) were studied. It was shown differences in development enzyme systems of control and experimental animals during ontogenesis.
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PMID:[Experimental study of the effect of formaldehyde during embryogenesis on the activity of rat liver enzyme systems in ontogenesis]. 913 53

The terminal step in hepatic gluconeogenesis is catalyzed by glucose-6-phosphatase, an enzyme activity residing in the endoplasmic reticulum and consisting of a catalytic subunit (glucose-6-phosphatase (G6Pase)) and putative accessory transport proteins. We show that Zucker diabetic fatty rats (fa/fa), which are known to exhibit impaired suppression of hepatic glucose output, have 2.4-fold more glucose-6-phosphatase activity in liver than lean controls. To define the potential contribution of increased hepatic G6Pase to development of diabetes, we infused recombinant adenoviruses containing the G6Pase cDNA (AdCMV-G6Pase) or the beta-galactosidase gene into normal rats. Animals were studied by one of three protocols as follows: protocol 1, fed ad libitum for 7 days; protocol 2, fed ad libitum for 5 days, fasted overnight, and subjected to an oral glucose tolerance test; protocol 3, fed ad libitum for 4 days, fasted for 48 h, subjected to oral glucose tolerance test, and then allowed to refeed overnight. Hepatic glucose-6-phosphatase enzymatic activity was increased by 1.6-3-fold in microsomes isolated from AdCMV-G6Pase-treated animals in all three protocols, and the resultant metabolic profile was similar in each case. AdCMV-G6Pase-treated animals exhibited several of the abnormalities associated with early stage non-insulin-dependent diabetes mellitus, including glucose intolerance, hyperinsulinemia, decreased hepatic glycogen content, and increased peripheral (muscle) triglyceride stores. These animals also exhibited significant decreases in circulating free fatty acids and triglycerides, changes not normally associated with the disease. Our studies show that overexpression of G6Pase in liver is sufficient to perturb whole animal glucose and lipid homeostasis, possibly contributing to the development of metabolic abnormalities associated with diabetes.
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PMID:Perturbation of fuel homeostasis caused by overexpression of the glucose-6-phosphatase catalytic subunit in liver of normal rats. 981 78