Disease relevance of NSC6495

• Infarct size was measured from cumulative release of alpha-hydroxybutyrate dehydrogenase, and left ventricular function was assessed by contrast angiograms 10 days after the infarction [1].
• The method is applied to creatine kinase (CK) and alpha-hydroxybutyrate dehydrogenase (HBDH) plasma activities in 36 patients with acute myocardial infarction (AMI) [2].
• Release of alpha hydroxybutyrate from neonatal rat heart cell cultures exposed to anoxia and reoxygenation: comparison with impairment of structure and function of damaged cardiac cells [3].
• Monitoring by alpha-hydroxybutyrate dehydrogenase of human ovarian carcinoma grown in nude mice [4].
• The absolute configuration of urinary 2-hydroxybutyric acid in patients with ketosis and lactic acidosis [5].

Psychiatry related information on NSC6495

• In this study, for determining the influence of different life style on the serum alpha hydroxybutyrate dehydrogenase activity (alpha HBD), we carried out surveys and laboratory studies on the relationships of the nutritional intake, physical activity, cigarette smoking and alcohol consumption of young females with their serum alpha HBD activity [6].

High impact information on NSC6495

• No difference between the treatment groups was observed in infarct size estimated from myocardial release of alpha-hydroxybutyrate dehydrogenase or in left ventricular ejection fraction after 10-22 days [7].
• Plasma activities of creatine kinase (CK) and alpha-hydroxybutyrate dehydrogenase (HBD) were measured after permanent coronary artery occlusion in the dog [8].
• The activity of alpha-hydroxybutyrate dehydrogenase in the original tumor was similar to that in the tumor grown in nude mice, while the activity in the cultured cells was about 2.5 times higher than those in both original tumor and the tumor grown in nude mice [9].
• METHODS: The primary efficacy end point was the infarct size measured by the cumulative release of alpha-hydroxybutyrate dehydrogenase (alpha-HDBH) (area under the curve [AUC] 0 to 72 h) [10].
• The analyses were carried out under optimized conditions, using a buffer system composed of 15 mM benzoate and 0.5 mM cetyltrimethylammonium bromide at pH 6.0, and 25% v/v methanol; 2-hydroxybutyric acid was selected as the internal standard (IS) [11].

Chemical compound and disease context of NSC6495

• During the three days after an infarction, lactate and alpha-hydroxybutyrate dehydrogenase can provide diagnostic thresholds of constant sensitivity and specificity [12].
• Serial measurements of haematocrit (Ht), plasma thyroxine (T4), triiodothyronine (T3) and alpha-hydroxybutyrate dehydroxygenase (alpha-HBDH) were performed in patients following myocardial infarction (MI) [13].
• Cytoplasmic lactate dehydrogenase (LDH), alpha-hydroxybutyrate dehydrogenase (HBDH), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) enzymatic activities were measured in normal renal cortical tissue and in hypernephroma [14].

Biological context of NSC6495

• The loss of cell viability was expressed as percentage decrease of the fluorescence at 360 nm (the calcium independent wavelength), since the percent release of cellular alpha-hydroxybutyrate dehydrogenase (alpha-HBDH) activity equalled the percent decrease of the fluorescence at 360 nm [15].
• This problem was studied by determination of the plasma isoenzyme activities of creatine kinase, lactate dehydrogenase, aspartate aminotransferase and alpha-hydroxybutyrate dehydrogenase in patients after cardiac surgery and after acute myocardial infarction [16].
• The results indicate an impairment of mitochondrial energy metabolism caused by 2-hydroxybutyric acid, a fact that may secondarily lead to reduction of lipid synthesis [17].
• To assess the value of alpha-hydroxybutyrate dehydrogenase (alpha-HBDH) in the diagnosis of painful crisis (PC) of sickle cell anaemia (SCA), we studied plasma enzyme levels in 55 children with HbSS and 21 control subjects with haemoglobin genotype AA [18].
• At the same time there were significant increases in organ weight (lungs and kidneys), and in exudate to thorax, hematocrit, and serum biochemical patterns (glucose, phosphorus, uric acid, blood urea nitrogen, glutamic pyruvic transaminase, glutamic oxaloacetic transaminase and alpha-hydroxybutyrate dehydrogenase) [19].

Anatomical context of NSC6495

• Therefore, activities of creatine kinase (CK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alpha-hydroxybutyrate dehydrogenase (alpha-HBDH) were determined in the plasma and left ventricular myocardium of rats following local heart irradiation with a single dose of 20 Gy [20].
• In order to establish that the tumor burden in nude mice bearing a xenografted human ovarian tumor can be assessed by measuring plasma levels of alpha-hydroxybutyrate dehydrogenase (HBD) (E.C. 1.1.1.30), the plasma HBD and the tumor volume were measured every week after inoculation of a human ovarian carcinoma cell line designated HR [4].
• Identification of 2-hydroxybutyric acid in human amniotic fluid [21].
• We also demonstrated a significant inhibition of lipid synthesis (20-45%) in cerebral cortex prisms and total homogenates in the presence of 2-hydroxybutyric acid [17].
• The enzymatic activities of lactate dehydrogenase (LDH) and alpha-hydroxybutyrate dehdyrogenase (HBDH) were measured in 87 semen samples [22].

Associations of NSC6495 with other chemical compounds

• The serum activities of creatine kinase (CPK), aldolase (ALD) and alpha-hydroxybutyrate dehydrogenase (HBD) were determined in a group of Welsh Mountain ponies before and after a 30 minute period of neuroleptanalgesia induced by i.v. injection of Immobilon and terminated by i.v. injection of Revivon [23].
• Serum levels of Lactate Dehydrogenase (LDH), alpha-Hydroxybutyrate Dehydrogenase (HBDH) and the relative ratio of alpha-Hydroxybutyrate Dehydrogenase to Lactate Dehydrogenase (HBDH/LDH) were determined in 51 cases of histologically proved testicular germ cell tumors and 40 healthy controls [24].
• CO2 production was significantly inhibited (30-70%) by 2-hydroxybutyric acid in cerebral cortex prisms, in total homogenates and in the mitochondrial fraction [17].
• Plasma creatine kinase (CK), creatine kinase isoenzyme MB (CK-MB), lactate dehydrogenase (LDH), alpha-hydroxybutyrate dehydrogenase (HBDH), glutamic-oxaloacetic transaminase (GOT), malondialdehyde (MDA) concentrations, and superoxide dismutase (SOD) activity were measured [25].
• PLP concentrations were higher in the air-GLc group than in the air group. alpha-Hydroxybutyrate dehydrogenase (alpha-HBDH) and creatine kinase (CK) leakages were observed in the N2 group, whereas 1.17 +/- 0.17 mM GLc prevented leakage [26].

Gene context of NSC6495

• Cumulative plasma release of creatine kinase (CK) and alpha-hydroxybutyrate dehydrogenase (HBD) was compared with release of alanine aminotransferase (ALT) [27].
• METHODS: Concentrations of FABP and MYO and, for comparison, activities of the established cardiac markers, creatine kinase (CK) and alpha-hydroxybutyrate dehydrogenase (HBDH), were assayed in serial plasma samples from 138 patients with AMI [28].
• For treatment and prognostic evaluation of patients with measles, it is important to determine the source of the increase in serum alpha-hydroxybutyrate dehydrogenase (HBD; EC 1.1.99.6) [29].
• In 87 patients with STEMI undergoing primary PCI, serial plasma concentrations of cTnI and alpha-hydroxybutyrate deshydrogenase (HBDH) were measured before PCI and over the following 72 h [30].
• Plasma levels of H-FABP were compared with plasma activity levels of the myocardial cytoplasmic enzymes creatine kinase MB (CK-MB) and alpha-hydroxybutyrate dehydrogenase (alpha-HBDH) [31].

Analytical, diagnostic and therapeutic context of NSC6495

• Enzymatic infarct size, as measured from cumulative alpha-hydroxybutyrate dehydrogenase release, was smaller in patients allocated to thrombolytic therapy (median 760 vs 1170 U/liter in control patients, p = .0001) [32].
• Cumulative 72-h release of alpha-hydroxybutyrate dehydrogenase (HBDH) and global ejection fraction derived from angiography and nuclear scintigraphy were used as independent measures of infarct size [33].
• BACKGROUND: Estimation of infarct size with serum-time activity curves of creatine kinase (CK) (or CKMB) or alpha-hydroxybutyrate dehydrogenase (HBDH) is widely used in clinical trials [34].
• 1. The formation of 2-hydroxybutyric acid (2-HB) has been studied by animal experiments [35].
• Urine and blood samples from patients with different clinical disorders were examined for 2-hydroxybutyric acid (2-HB) by gas chromatography and mass spectrometry [36].

References