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

A virulent fish strain of Aeromonas hydrophila was inoculated intramuscularly into laboratory mice (B10.G strain). Histological, biochemical and haematological changes during the first 36 h of the infection were measured. Inoculation led to septicaemia, tissue damage, endotoxic shock and death. Histological examination revealed: (1) severe muscle necrosis at the injection site; (2) oedema, haemorrhage and neutrophil infiltration of the lung; and (3) focal parenchymal necrosis in the liver. Significant increases in aspartate aminotransferase, alanine aminotransferase, intestinal bilirubin and blood urea nitrogen were noted in blood and intestinal samples; decreased plasma glucose and haematological changes were also recorded. Ketones, increased protein, glucose, bilirubin and blood were detected in the urine. Endotoxaemia was demonstrated as early as 2 h after inoculation and persisted for more than 36 h. The changes resembled those described for certain other experimental infections in laboratory animals. Our results suggest that endotoxin contributed to the pathogenesis of aeromonas infection in mice.
 ...
PMID:Pathophysiology of experimental Aeromonas hydrophila infection in mice. 372 83

To determine organ damage due to hypoglycemia, we studied the effects of insulin dose and hypoglycemia duration on serum enzyme activity in rabbits. Thirty rabbits were randomly divided into five groups according to hypoglycemia duration and insulin dose: A2, hypoglycemia for 30 minutes with 2 U/kg insulin; A10, hypoglycemia for 30 minutes with 10 U/kg insulin; B2, hypoglycemia for 60 minutes with 2 U/kg insulin; B10, hypoglycemia for 60 minutes with 10 U/kg insulin; and C, no hypoglycemia with 10 U/kg insulin and 50% glucose. Insulin-induced hypoglycemia was reversed by intravenous injection of glucose. Alterations in serum enzyme activity and creatine kinase (CK) isoenzyme distribution were determined before and after insulin injection. Serum CK activity increased significantly in all hypoglycemic groups compared with preinjection values, and tended to remain high for 24 hours in both groups A10 and B10. Serum activity of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) increased only in group B10. In addition, the level of band 4 of serum CK isoenzymes, which exists predominantly in skeletal muscle and myocardium, increased significantly in group B10. These results suggest that the increase in both serum enzyme and CK band 4 isoenzyme activities during hypoglycemia is primarily due to damage in muscle rather than liver, and that the hypoglycemia duration and insulin dosage may influence the extent of organ damage.
 ...
PMID:Muscle damage induced by experimental hypoglycemia. 986 76

The effects of cadmium stress on growth, morphology, and protein expression were investigated in Rhodobacter capsulatus B10 using two-dimensional polyacrylamide gel electrophoresis and a scanning electron microscope with an energy dispersive X-ray spectrometer. The bacterium grew in the presence of 150 microM CdCl2 and highly induced heat-shock proteins (GroEL and Dnak), S-adenosylmethionine synthetase, ribosomal protein S1, aspartate aminotransferase, and phosphoglycerate kinase. Interestingly, the ribosomal protein S1 was proportionally expressed as the amount of cadmium in the medium, suggesting that S1 may be required for the repair of cadmium-mediated cellular damage. On the other hand, we identified five cadmium-binding proteins: 2-methylcitrate dehydratase, phosphate periplasmic binding protein, inosine-5'-monophosphate dehydrogenase/guanosine-5'-monophosphate reductase, inositol monophosphatase, and lytic murein transglycosylase. The cadmium-treated cells had a filamentous structure and contained less phosphorous than the untreated cells. We propose that these characteristics of the cadmium-treated cells may be due to the inactivation of the phosphate periplasmic binding protein and lytic murein transglycosylase by cadmium.
 ...
PMID:Effects of cadmium stress on growth, morphology, and protein expression in Rhodobacter capsulatus B10. 1703 Oct 48