Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.9 (glucose-6-phosphatase)
 3,081 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rats exposed to cosmetic kerosene mists (odourless kerosene), concentration of 75 and 300 mg/m3 for 14 days, underwent morphological and cytoenzymatic liver tests and biochemical tests of lipids composition in this organ. In addition, lipids concentration and activity of test--enzymes in blood serum were determined. The findings were: passive congestion, fine--droplet fatty degeneration in I zones of clusters and increased number of Browicz--Kupffer's phagocytes near liver triads. Those changes were accompanied by: decreased activity of succinic dehydrogenese (SDH), tetrazolic NADPH--reductase (NADPH-r.t.) and glucose-6-phosphatase (G-6-P-ase) and increased activity of adenosine triphosphatase (Mg++-ATP-ase) and acid phosphatase (AcP). In blood serum medium increase of base phosphatase (AP), 5-nucleotidase (5-Nt) and leucyloaminepeptidase (LAP) and decreased activity of prothrombin (Pt) were found. In addition, it was demonstrated that liver steatosis was characterized by cumulation of free fatty acids, phospholipids and cholesterol esters with simultaneous decrease in triglycerides content in this organ. The obtained results indicate that changes induced by kerosene hydrocarbons in liver are focal and cumulate in I zones of liver clusters. The degree of lesion varies with the extent of exposure, and results from toxic effects of this preparation on hepatic cells lypoproteid membranes.
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PMID:[Comparative studies on the toxicity of various dieelectrics, kerosene derivatives, used in the electroerosion technic. I. Morphological, cytoenzymatic and biochemical changes in the liver of rats chronically exposed to kerosene hydrocarbons]. 630 48

A flock of Rambouillet sheep was examined because of increased lamb mortality caused by ineffective hemostasis at parturition. Neonatal-affected lambs presented with inadequate hemostasis at the umbilicus, pale mucus membranes, and markedly prolonged activated clotting time. Affected lambs had consistently prolonged 1-stage prothrombin times and activated partial thromboplastin times that supported a defect in the common pathway or defects in both the intrinsic and extrinsic pathway of the coagulation cascade. Decreased activity of vitamin K-dependent procoagulant factors II, VII, IX, and X in male and female lambs suggested either a defect of the hepatic enzyme gamma-glutamyl carboxylase, or vitamin K(1) 2,3 epoxide reductase. Affected lamb hepatic gamma-glutamyl carboxylase activity was markedly decreased compared with that of age- and sex-matched control lambs, while vitamin K(1) 2,3 epoxide reductase and glucose-6-phosphatase activities were similar between an affected and normal lamb. Subcutaneous vitamin K(1) supplementation did not increase vitamin K-dependent procoagulant factor activities in 3 lambs administered vitamin K(1) daily. These data confirm defective gamma-glutamyl carboxylase activity as the cause of impaired coagulation of sheep in this flock. This flock represents the only viable animal model of hereditarily defective gamma-glutamyl carboxylase activity.
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PMID:Defective gamma-glutamyl carboxylase activity and bleeding in Rambouillet sheep. 1696 51