Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study examines the role of cardiac lysosomal enzymes in the pathogenesis of the cardiomyopathy that develops in genetically diabetic C57BL/KsJ db+/db+ mice. Db+/db+ mice and littermate controls were sacrificed as age-matched pairs between 5-26 weeks of age. C57BL/6J ob/ob mice and littermates served as other controls. The hearts were excised, homogenized, and the following enzymatic activities measured: N-Acetyl-beta-glucosaminidase, N-acetyl-beta-galactosaminidase, beta-glucosaminidase, aryl sulphatase, alpha-mannosidase, alpha-glucosidase, beta-galactosidase, beta glucosidase, total p-nitrophenyl phosphatase, acid phosphatase and 5'-phosphodiesterase type IV. There is a progressive decrease in cardiac lysosomal enzyme activities of db+/db+ mice for the period 5-21 weeks of age. All enzyme activity is depressed significantly during the 9-21 week interval with beta-glucuronidase, aryl sulphatase and beta-glucosidase decreased about 40-50%. The decrease in lysosomal enzyme activity can explain the accumulation of large residual bodies and interstitial material in the myocardium of the db+/db+ animals
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PMID:Lysosomal enzymes in experimental diabetic cardiomyopathy. 678 Feb 37

Muscular dystrophy and cardiomyopathy were produced in weanling rats by feeding a vitamin E-deficient diet for 12 mth. Deficient and control rats were killed, and skeletal muscle and myocardium were used for subcellular studies and biochemical assay of selected lysosomal enzymes. Ultrastructurally, the skeletal muscle showed various degrees of pathological changes. In the severely damaged muscle fibres, prominent increase of secondary lysosomes, autophagic vacuoles, residual bodies, disappearance of myofilaments, rupture of sarcolemma and shrinkage of muscle fibres were noted. The damaged muscle fibres finally became dense residual bodies and dispersed in the interstitial spaces, where the macrophages and fibroblasts were found. In the myocardium, some muscle fibres were intact with mild fatty infiltration and marked proliferation of mitochondria. However, in the severely damaged myocardial fibres, the whole fibre was always filled with amorphous dense bodies, and the sarcolemma was ruptured. This resulted in dispersion of many cellular organelles in the surrounding interstitial space. A significant increase of cathepsin and beta-glucuronidase activity in the cytosol of both organs suggests that lysosomal enzymes may play a major role in the destruction of muscle and cardiac fibres in the long-term vitamin E-deficient animals.
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PMID:Ultrastructural and lysosomal enzyme studies of skeletal muscle and myocardium in rats with long-term vitamin E deficiency. 715 34