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

This study was aimed to evaluate the preventive effect of gallic acid on lysosomal enzymes in isoproterenol treated myocardial infarcted rats. Male albino Wistar rats were pretreated with gallic acid (15 mg/kg) daily for a period of 10 days. After the treatment period, isoproterenol (100 mg/kg) was subcutaneously injected to rats twice at an interval of 24 h. The activity of creatine kinase-MB and lactate dehydrogenase were increased significantly (P<0.05) in the serum of isoproterenol induced cardiotoxic rats. The levels of lipid peroxidation products (thiobarbituric acid reactive substances, lipid hydroperoxides) were significantly (P<0.05) increased and the level of reduced glutathione was significantly (P<0.05) decreased in the plasma and heart of isoproterenol induced cardiotoxic rats. The activities of lysosomal enzymes (beta-glucuronidase, beta-N-acetylglucosaminidase, beta-galactosidase, cathepsin-B and D) were increased significantly (P<0.05) in the serum and heart of isoproterenol induced cardiotoxic rats. Isoproterenol induction also resulted in decreased stability of membranes, which was reflected by lowered activities of beta-glucuronidase and cathepsin-D in lysosomal fraction. Pretreatment with gallic acid (15 mg/kg) to isoproterenol treated rats significantly (P<0.05) prevented the changes in the activities of cardiac marker enzymes, the levels of lipid peroxidation products, reduced glutathione and the activities of lysosomal enzymes. Oral treatment with gallic acid (15 mg/kg) to normal control rats did not show any significant effect. Thus, the results of our study show that gallic acid prevents the lysosomal membrane damage against isoproterenol induced cardiac damage and brought back the activities of lysosomal enzymes to near normal levels. The observed effects of gallic acid are due to antilipoperoxidative and antioxidant effects.
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PMID:Gallic acid prevents lysosomal damage in isoproterenol induced cardiotoxicity in Wistar rats. 1945 May 77

This paper reviews different techniques for analyzing the transfection efficiencies and cytotoxicities of dendriplexes-complexes of nucleic acids with dendrimers. Analysis shows that three plasmids are mainly used in transfection experiments: plasmid DNA encoding luciferase from the firefly Photinus pyralis, beta-galactosidase, or green fluorescent protein. The effective charge ratio of transfection does not directly correlate with the charge ratio obtained from gel electrophoresis, zeta-potential or ethidium bromide intercalation data. The most popular cells for transfection studies are human embryonic kidney cells (HEK293), mouse embryonic cells (NIH/3T3), SV40 transformed monkey kidney fibroblasts (COS-7) and human epithelioid cervical carcinoma cells (HeLa). Cellular uptake is estimated using fluorescently-labeled dendrimers or nucleic acids. Transfection efficiency is measured by the luciferase reporter assay for luciferase, X-Gal staining or beta-galactosidase assay for beta-galactosidase, and confocal microscopy for green fluorescent protein. Cytotoxicity is determined by the MTT test and lactate dehydrogenase assays. On the basis of the papers reviewed, a standard essential set of techniques for characterizing dendriplexes was constructed: (1) analysis of size and shape of dendriplexes in dried/frozen state by electron or atomic force microscopy; (2) analysis of charge/molar ratio of complexes by gel electrophoresis or ethidium bromide intercalation assay or zeta-potential measurement; (3) analysis of hydrodynamic diameter of dendriplexes in solution by dynamic light scattering. For the evaluation of transfection efficiency the essential techniques are (4) luciferase reporter assay, beta-galactosidase assay or green fluorescent protein microscopy, and (5) cytotoxicity by the MTT test. All these tests allow the transfection efficiencies and cytotoxicities of different kinds of dendrimers to be compared.
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PMID:How to study dendriplexes II: Transfection and cytotoxicity. 1981 39

We evaluated the preventive effect of caffeic acid (CA) on lysosomal enzymes in isoproterenol (ISO)-treated myocardial infarcted rats. Male albino Wistar rats were pretreated with CA (15 mg/kg) daily for a period of 10 days. After the pretreatment period, ISO (100 mg/kg) was subcutaneously injected to rats twice at an interval of 24 h. The activity of serum creatine kinase-MB and lactate dehydrogenase was increased significantly (P < 0.05) in ISO-induced myocardial infarcted rats. The levels of plasma thiobarbituric acid reactive substances and lipid hydroperoxides were significantly (P < 0.05) increased, and the level of plasma-reduced glutathione was significantly (P < 0.05) decreased in ISO-induced myocardial infarcted rats. The activities of lysosomal enzymes (beta-glucuronidase, beta-N-acetylglucosaminidase, beta-galactosidase, cathepsin-B and cathepsin-D) were increased significantly (P < 0.05) in the serum and heart of ISO-induced myocardial infarcted rats. ISO induction also resulted in decreased stability of membranes, which was reflected by lowered activities of beta-glucuronidase and cathepsin-D in different fractions except cytosol. Pretreatment with CA (15 mg/kg) to ISO-treated rats significantly (P < 0.05) prevented the changes in the activities of cardiac marker enzymes, the levels of lipid peroxidation products, reduced glutathione and the activities of lysosomal enzymes in the serum, heart, and subcellular fractions. Oral treatment with CA (15 mg/kg) to normal control rats did not show any significant effect. Thus, the results of our study showed that CA prevented the lysosomal membrane damage against ISO-induced myocardial infarction. The observed effects of CA are due to membrane-stabilizing, antilipo peroxidative, and antioxidant effects.
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PMID:Preventive effect of caffeic acid on lysosomal dysfunction in isoproterenol-induced myocardial infarcted rats. 2039 26


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