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)

Adriamycin, which is widely used in the treatment of various neoplastic conditions, exerts toxic effects in many organs. The present study was designed to investigate the effect of lipoic acid upon adriamycin induced peroxidative damages in rat kidney. The increase in peroxidated lipids on adriamycin administration was accompanied by alterations in the antioxidant defense systems. The extent of nephrotoxicity induced by adriamycin was evident from the decreased activities of the enzymes gamma-glutamyl transferase and beta-glucuronidase in the rat renal tissues. The study was carried out with adult male albino rats of Wistar strain, which comprised of one control and three experimental groups. Group I rats served as controls. Group II rats received adriamycin (1 mg kg(-1) body wt day(-1)) intravenously through the tail vein. Group III rats were given lipoic acid (35 mg kg(-1) body wt day(-1)) intraperitoneally. Group IV rats were given lipoic acid 24 h before the administration of adriamycin. Rats subjected to adriamycin administration showed a decline in the thiol capacity of the cell accompanied by high malondialdehyde levels along with lowered activities of catalase, superoxide dismutase, glutathione peroxidase and glutathione metabolizing enzymes (glutathione reductase, glucose-6-phosphate dehydrogenase, glutathione-S-transferase). Lipoic acid pretreatment also restored the activities of gamma-glutamyl transferase and beta-glucuronidase nearly to control levels thereby suggesting nephroprotection. The study has highlighted the beneficial effects of lipoic acid pretreatment in reversing the damages caused by adriamycin and thereby bringing about an improvement in the oxidative stress parameters.
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PMID:Protective effect of lipoic acid on adriamycin induced lipid peroxidation in rat kidney. 1284 25

This study examined the effects of estrogen supplementation on markers of neutrophil infiltration and damage in skeletal muscle of rats following ischemia. Male and female gonad-intact rats, with or without 14 days of estrogen supplementation were subjected to two hours of hind-limb ischemia and sacrificed at 24, 48 or 72 hours post-ischemia. Control animals were sacrificed without ischemia. Plantaris and red and white gastrocneimus muscles were removed and assayed for myeloperoxidase (MPO), a marker of neutrophil infiltration, and glucose-6-phosphate dehydrogenase (G6PD) and beta-glucuronidase (betaGLU), as markers of muscle damage. Significant elevations of MPO, G6PD and betaGLU activities were observed at various time points post-ischemia. No systematic differences between genders were noted in any of the measures. Estrogen supplementation in both male and female animals failed to significantly attenuate post-ischemia increases in MPO, G6PD and betaGLU activities in any of the muscles studied and in some cases accentuated activities of some of these measures. Unlike previous findings following exercise in skeletal muscle, this study failed to demonstrate estrogen-induced attenuation of indices of neutrophil infiltration or damage in skeletal muscles of rats up to 72 hours following ischemia. This demonstrates that estrogen may not consistently attenuate neutrophil infiltration and that a number of variables including damage modality, tissue or estrogen level may influence this.
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PMID:Estrogen supplementation failed to attenuate biochemical indices of neutrophil infiltration or damage in rat skeletal muscles following ischemia. 1623

Lysosomal changes of mouse skeletal muscle during the repair of exercise injuries were studied with biochemical, histochemical, and electron microscopic methods. Treadmill running for 4 hours and 9 hours increased the activities of cathepsin C and beta-glucuronidase, but not that of beta-glycerophosphatase in mouse quadriceps femoris muscle. The highest activities occurred 3 days after exertion and were higher after the longer duration of exertion. Similar changes that were highly correlated with the activities of lysosomal enzymes occurred in the activities of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase and in the concentration of DNA. The activities of lysosomal enzymes correlated significantly with the severity of histopathologic injuries. Histochemical stainings of beta-N-acetylglucosaminidase and beta-glucuronidase showed a strong increase in the staining intensity 3 and 5 days after exertion, both in inflammatory phagocytes and in surviving muscle fibers in the injured area, and staining intensities increased in parallel with the severity of injuries. Electron microscopy showed an increased number of autophagic vacuoles, lysosome-like bodies, and Golgi complexes in the fibers adjacent to necrotic foci, coinciding with the highest histochemical staining pattern. Lysosomal changes in surviving muscle fibers in close proximity to injured muscle fibers could, by autophagic degradation, provide structural elements for the regeneration of injured muscle fibers.
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PMID:Lysosomal changes in mouse skeletal muscle during the repair of exercise injuries. 1675 92


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