Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We measured creatine kinase (EC 2.7.3.2) activity in 1009 serum samples from 538 patients in the intensive-care units of the University of Texas Medical Branch hospitals. Creatine kinase isoenzymes migrating cathodal to skeletal muscle creatine kinase (CK-MM) on cellulose acetate electrophoresis were found in sera from 14 of the 538 patients. Creatine kinase, lactate dehydrogenase (EC 1.1.1.27), aspartate aminotransferase (EC 2.6.1.1), and alanine aminotransferase (EC 2.6.1.2) activities were abnormally increased in these 14 patients. Liver lactate dehydrogenase isoenzyme (LDH5) and cardiac creatine kinase isoenzyme (CK-MB) were abnormally increased in 12 and eight of these patients, respectively. Ten of the 14 patients died during their hospital admission. We believe the creatine kinase isoenzymes that migrated cathodal to skeletal muscle creatine kinase (CK-MM) were of mitochondrial origin.
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PMID:Creatine kinase isoenzymes of mitochondrial origin in human serum. 44 29

We have used the W.H.O. International Reference Venom from the Australian tiger snake, Notechis scutatus, to study possible methods for the assessment of local myonecrosis caused by this venom. We made subcutaneous injections of various doses (0.25-20.0 micrograms) of venom into the antero-lateral aspect of the rat hind limb. The soleus muscle was removed after 24 hr and muscle fibre loss calculated from photo-montages of histological sections. Muscle tissue which had been either frozen or wax-embedded was preferable to resin-embedded tissue for making muscle fibre counts. There was a dose-dependent relationship between muscle fibre loss and the amount of venom inoculated. One microgramme of crude venom caused the loss of 50% of muscle fibres from the soleus muscle. This dose of venom neutralized by 1.5 microliters of the W.H.O. International Standard Antivenom for Notechis scutatus. Muscle wet weight increased following the inoculation of venom, to reach a peak of 42% at a dose of 0.5 microgram. There was no correlation between fibre loss and increase in wet weight. Biochemical analysis of both the venom-damaged muscle and the plasma showed that there was a strong linear correlation (r = 0.95) between loss of muscle aspartate aminotransferase and muscle fibre loss. There was a non-linear relationship between muscle fibre loss and the increase of plasma aspartate aminotransferase (EC 2.6.1.1). There was no correlation between either the loss of muscle creatine kinase or the increase of plasma creatine kinase and muscle fibre loss. We conclude that direct measurements are required to calculate muscle fibre loss with precision, but that the loss of muscle aspartate aminotransferase AST and its release into the plasma may also be important criteria to be used when studying local necrosis.
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PMID:The assessment of muscle fibre loss after the injection of the venom of Notechis scutatus (Australian tiger snake). 169 44

The use of sensitive biomarkers to monitor skeletal muscle toxicity in preclinical toxicity studies is important for the risk assessment in humans during the development of a novel compound. Skeletal muscle toxicity in Sprague Dawley Rats was induced with clofibrate at different dose levels for 7 days to compare standard clinical pathology assays with novel skeletal muscle and cardiac muscle biomarkers, gene expression and histopathological changes. The standard clinical pathology assays aspartate aminotransferase (AST), alanine aminotransferase (ALT), and creatine kinase (CK) enzyme activity were compared to novel biomarkers fatty acid binding protein 3 (Fabp3), myosin light chain 3 (Myl3), muscular isoform of CK immunoreactivity (three isoforms CKBB, CKMM, CKMB), parvalbumin (Prv), skeletal troponin I (sTnI), cardiac troponin T (cTnT), cardiac troponin I (cTnI), CKMM, and myoglobin (Myo). The biomarker elevations were correlated to histopathological findings detected in several muscles and gene expression changes. Clofibrate predominantly induced skeletal muscle toxicity of type I fibers of low magnitude. Useful biomarkers for skeletal muscle toxicity were AST, Fabp3, Myl3, (CKMB) and sTnI. Measurements of CK enzyme activity by a standard clinical assay were not useful for monitoring clofibrate-induced skeletal muscle toxicity in the rat at the doses used in this study.
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PMID:Biomarker evaluation of skeletal muscle toxicity following clofibrate administration in rats. 2702 44