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 lysosomotropic agent--sodium aurothiomalate on liver damage and lysosomal changes during acute toxic hepatitis was studied. Combined administration of sodium aurothiomalete led to less extensive necrosis and to widening dystrophic areas in the hepatic parenchyma. Solubilization of the acid RNA-ase activity was decreased, and nonsedimentable activities of beta-galactosidase, cathepsin D were the same as in acute CCl4-hepatitis.
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PMID:[Effect of sodium aurothiomalate in acute toxic hepatitis]. 40 45

Physical and chemical properties of the rat liver lysosomes with single Triton WR 1339 overloading were studied during the administration of a detergent to intact rats and those with acute toxic hepatitis. Administration of the latter to intact animals was accompanied by a reduction of the floating density of the particles, solubilization of the lysosome enzymes and by increased fragility of the particles in the hypotonic medium. Lysosomes of the hepatocytes in rats with toxic hepatitis also displayed signs of overloading of the vacuolar apparatus with the preparation administered. The most pronounced solubilization of the lysosomal enzymes beta-galactosidase, acid RNA-ase, cathepsin D--was noted in case of combined action of CCl4 and Triton WR 1339 24, 48, 72 hours and 7 days after the CCl4 poisoning. Possible consequences of overloading of the vacuolar apparatus of the rat hepatocytes are discussed.
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PMID:[Role of vacuolar apparatus overload in lysosomal changes in liver cells in acute toxic hepatitis]. 42 73

Structural and functional changes in the dog liver and regional lymph nodes lysosomes were studied during toxic hepatitis induced by CCl4 administration (single and repeated). Total activity of lysosomal enzymes (acid RNA-ase and beta-galactosidase) was higher in the regional lymph nodes than in the liver, reflecting the barrier, protective function of the organ. During acute toxic hepatitis the specific activities of acid RNA-ase and cathepsin D displayed a sharp rise. No normalization of the indices under study occurred during the observation period (from 8 to 30 days). At the same time there was a rise of the regional lymph node weight and an elevation of the relative macrophage and neutrophil content in the sinuses. The increased activity of the lysosome enzymes in the regional lymph nodes in injury of the liver was connected with greater functional load on the lymph nodes effecting hydrolysis of biopolymeres which penetrated into the regional lymphatic node with the lymph.
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PMID:[Structuro-functional changes in dog liver and regional lymph node lysosomes in toxic hepatitis]. 70 70

Changes in activities of a new proteinase cathepsin T as well as some other lysosomal acid proteinases and hydrolases were examined in liver homogenate from rats treated with a single hepatotoxic dose of carbon tetrachloride. The most striking changes were several-fold increases of liver cathepsin T and D activities over their levels in untreated rats 3 days after administration of the agent to rats. Increase of cathepsin T was greater than that of cathepsin D at all doses of the hepatotoxin examined. The activities of N alpha-benzoyl-DL-arginine 2-naphthylamide hydrolase, acid phosphatase, beta-galactosidase and beta-glucuronidase in poisoned rat liver were unchanged or only slightly increased. Cathepsin T and D activities were less enhanced in mitochondrial lysosomal fractions than in the homogenate, and were greatly elevated in the supernatant fractions of liver from the treated rats. As judged from the molecular weights, the elevated activities of cathepsins T and D in the treated rat liver could be attributable to the two cathepsins themselves and not to other proteinases. Administration to rats of other hepatotoxic agents, thioacetamide and dimethylnitrosamine, also induced the elevation of the two cathepsin activities in liver, but on partial hepatectomy the activities of liver cathepsins T and D did not show such marked increases. Nonparenchymal liver cell fractions were responsible for almost all the increased activities of liver cathepsins T and D. It is possible that cathepsins T and D play a role in the heterolytic breakdown of hepatocyte molecules following CCl4 poisoning.
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PMID:Increased activities of liver cathepsins T and D in carbon tetrachloride-treated rats. 649 24

Liver tissue cirrhosis, developed in rats after long-term administration of CCl4, led to distinct increase in activities of acid phosphatase, acid DNAase, cathepsin D, beta-galactosidase and beta-glucosidase. When the treatment with the hepatotropic toxins was stopped activity of lysosomal enzymes decreased slightly but was maintained at the high level. Within a day after a single administration of choriogonine distinct decrease as compared with the controls in activity of all the acid hydrolases studied was found. Within subsequent periods the lysosomal enzymes activity continued to decrease and within 2 months after the choriogonine treatment it was distinctly lower as compared with control animals.
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PMID:[Effect of choriogonine on the enzymatic activity of lysosomes in the cirrhotic liver in the rat]. 681 64

We previously identified the promoter sequence that is essential for basal and TGF-beta-stimulated transcription of alpha2(I) collagen gene (COL1A2). In the present study, we examined whether the promoter is activated during hepatic fibrogenesis by utilizing transgenic mice harboring the COL1A2 upstream sequence. Intraperitoneal CCl4 administration activated the -17 kb COL1A2 promoter more than 10-fold, whereas partial hepatectomy resulted in no significant change in the promoter activity. The non-parenchymal cell fraction, but not parenchymal hepatocytes, isolated from mice harboring the -313 COL1A2 promoter linked to a beta-galactosidase reporter gene contained large amounts of beta-galactosidase and endogenous COL1A2 mRNAs. beta-galactosidase activity in the cells from CCl4-treated mice was significantly higher than in those from untreated animals. These results indicated that different molecular mechanisms control COL1A2 transcription in CCl4-induced liver injury/fibrosis and physiological regeneration after partial hepatectomy, and that the -313 COL1A2 promoter is activated in a cell type-specific manner during hepatic fibrogenesis.
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PMID:Activation of Proalpha2(I) collagen promoter during hepatic fibrogenesis in transgenic mice. 978 93

We have tested the ability of bone marrow (BM) cells (BMCs) to form hepatocytes in liver injury models. We used three models: (i) carbon tetrachloride (CCl4) treatment, (ii) albumin-urokinase transgenic mouse [TgN(Alb1Plau)], and (iii) hepatitis B transgenic mouse [TgN(Alb1HBV)]. As a nonselective liver injury model, irradiated C57BL/6 (B6) mice were transplanted with BMCs from GFP transgenic mouse [TgN(ActbEGFP)] or beta-galactosidase transgenic mouse [TgN(MtnLacZ)] followed by the administration of CCl4. Irradiated TgN(Alb1HBV) and TgN(Alb1Plau) were also transplanted with BMCs from TgN(ActbEGFP) or TgN(MtnLacZ). Approximately 1.5 x 106 hepatocytes per liver were analyzed for GFP-positive cells, and the whole livers were inspected for beta-galactosidase expression. No GFP-positive hepatocytes and no gross blue staining of the livers with 5-bromo-4-chloro-3-indolyl beta-d-galactoside in any of the 18 recipient mice analyzed were detected. The livers from female animals with gender-mismatched BM transplantation were also tested with Y chromosome fluorescent in situ hybridization analysis to detect donor-derived cells. A total of five isolated hepatocytes were positive for Y chromosome in 4.1 x 105 hepatocytes analyzed. Our results demonstrate that there is little or no contribution of BMCs to the replacement of injured livers in these models. We conclude that BM-derived cells cannot generally lead to a cure of liver damage.
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PMID:Little evidence of bone marrow-derived hepatocytes in the replacement of injured liver. 1523 8