Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.1.1 (hexokinase)
 5,274 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe a new, nonenzymatic method for determining serum glucose. This method is based upon the direct electrochemical oxidation of glucose by means of stable nickel-catalyst that is electrodeposited onto a lead dioxide electrode surface. Linear calibration plots are obtained for glucose in the 0.1 to 4500 mg/liter range. Values for 23 sera with glucose concentrations ranging from 300 to 4300 mg/liter showed a linear correlation coefficient of 0.996 when compared with values reported by a hospital laboratory using the hexokinase method. Typically a 25-microliter sample is used, but samples as small as 5 microliter have been successfully analyzed. The sample is added to 25.00 ml of pH 13 electrolyte containing 1 mmol of NiSO4 per liter; the amount of increase in anodic current comproses the analytical signal. For 20 repetitive analyses of a serum specimen, the CV was less than 4%. Ascorbic acid is rapidly decomposed in the electrolyte used and thus does not interfere. Uric acid is inactive at the concentrations present in serum samples. The sensitivity and simplicity of the new method suggest it as an alternative to currently available procedures.
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PMID:Amperometric nonenzymatic determination of serum glucose by means of a nickel-catalyst electrode. 63 Jul 6

Wilson disease (WD) is an autosomal recessive disorder due to the defect in ATP7B gene characterized by excessive accumulation of copper in the liver with progressive hepatic damage and subsequent redistribution to various extrahepatic tissues including the brain, kidneys, and cornea. Strikingly, the total serum copper concentration is always low in WD, even though the non-ceruloplasmin copper level is still expected to be high. To assess the role of free radical reactions catalyzed by non-ceruloplasmin copper, we investigated erythrocyte metabolism and oxidative stress as a mechanism for hemolysis in eight WD patients during episodes of acute hemolysis and compared them with eight follow-up cases of WD on d-penicillamine therapy and eight healthy, age-matched children. Elevated levels of non-ceruloplasmin copper were found in all the WD patients during an episode of hemolytic anemia. There was marked inhibition in erythrocyte enzymes, namely, hexokinase, total adenosine triphosphatase (ATPase), and glucose-6-phosphate dehydrogenase (G-6-PD) from WD patients compared with patients on penicillamine and healthy children, indicating altered erythrocyte metabolism during a hemolytic crisis. Antioxidant status was also found to be compromised as is evident from decreased glutathione (GSH) levels, decreased antioxidant enzymes (namely, superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase), increased lipid peroxidation, and deranged plasma antioxidants. Uric acid showed maximum decrease followed by ascorbic acid. These findings suggest that the free radical production by elevated non-ceruloplasmin copper through transition metal catalyzed reactions leads to oxidative injury resulting in altered erythrocyte metabolism and severely compromised antioxidant status of WD patients during hemolytic anemia.
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PMID:Erythrocyte metabolism and antioxidant status of patients with Wilson disease with hemolytic anemia. 1654 36