Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This report describes a new specific colorimetric procedure for uric acid assay with AutoAnalyzer II and SMA (Technicon) systems, made specific by the application of uricase. Hydrogen preroxide, formed in this reaction, effects the oxidative coupling of 4-aminophenazone and 2,4-dichlorophenol under the catalytic influence of peroxidase. The red dye formed is measured at 505 or 520 nm. A sample blank measurement is not necessary, and the reagents show very good stability. The test shows linearity up to 714 mumol of uric acid per liter. Results of thie method correlate very well with those by the uricase-ultraviolet and uricase--catalase methods. There is no interference by hemoglobin, bilirubin, lipemia, and various drugs, except a minor interference by alpha-methyldopa. Interference from ascorbate is eliminated by ascorbate oxidase. This method can be regarded as a considerably improved routine test for uric acid on continuous-flow systems in clinical laboratories as compared with the commonly used phosphotungstate method.
 ...
PMID:Determination of uric acid on continuous-flow (AutoAnalyzer II and SMA) systems with a uricase/phenol/4-aminophenazone color test. 62 57

Studies are reported on the reaction kinetics of the glucose assay according to Trinder which involves the specific oxidation of glucose by glucose oxidase and the determination of the hydrogen peroxide released by means of phenol and 4-aminophenazone in the presence of peroxidase. The results have been used to develop a general kinetic fixed-time method for the analysis of glucose in whole blood and serum. The single reagent method has been adapted to the ENI GEMSAEC centrifugal analyzer and to the Abbott ABA-100 analyzer. The procedures exhibited excellent precision and the results correlated well with those obtained by the hexokinase method, Linearity was achieved from 3 to 64 mmol/1 glucose for the GEMSAEC method, and from 3 to 33 mmol/1 glucose for the ABA-100 method. Reagent or sample blank corrections were not necessary. There were no interferences from various drugs, hemoglobin, bilirubin, or lipemia.
 ...
PMID:Kinetic enzymatic method for automated determination of glucose in blood and serum. 83 60

We describe the effects of uric acid, hemolysis, drugs, ascorbic acid, lipemia, and bilirubin on the enzymic measurement of cholesterol in serum by use of reagent kits from Abbott, Beckman, Boehringer Mannheim, Calbiochem, and Worthington. In all of these, the chromogen formed from the reaction of hydrogen peroxide with phenol and 4-aminoantipyrene is measured. The absorbance was measured at 500 nm vs. a serum blank for each kit--except Abbott's with which the recorded absorbances were the differences between readings at 500 and 600 nm. With all reagents kits, there was no interference from uric acid up to 200 mg/liter, hemoglobin up to 1.0 g/liter, or drugs (clofibrate, phenobarbital, Ketochol, Ovral-28), but negative interferences from ascorbic acid. Except for the Abbott kit, the cholesterol values obtained for lipemic samples were lower than found with the comparison method [Abell et al., Stand. Methods Clin. Chem. 2, 26 (1958)]. With Abbott's reagents, for most lipemic samples, the values were the same. Bilirubin at concentrations of 200 mg/liter significantly decreased the cholesterol values with Beckman, Calbiochem, and Worthington reagent kits. With Boehringer Mannheim reagent a small negative interference was observed and with Abbott reagent a small positive interference was observed when the bilirubin concentrations were 200 mg/liter.
 ...
PMID:Interference with the enzymic measurement of cholesterol in serum by use of five reagent kits. 84 75

Ther are several main mechanisms that allow us to understand a number of the hepatic and metabolic effects of ethanol. Ethanol is oxidized in the liver to two products (hydrogen and acetaldehyde), to which many of the effects of ethanol can be attributed. The hydrogen generated alters the redox state, and though this effect is attenuated after chronic ethanol consumption, it may still be sufficient to explain alterations in lipid metabolism, possibly increased collagen deposition, and, under special circumstances, depression of protein synthesis. Acetaldehyde impairs microtubules, decreases protein secretion, and causes protein retention and ballooning of the hepatocyte. Acetaldehyde exerts toxicity also with regard to other key cellular functions, particularly in the mitochondria, and it may promote peroxidation of the cellular membranes. It is noteworthy that after chronic consumption of ethanol, there is increased acetaldehyde, in part because of decreased disposition in the mitochondria and partly because of induction of an alternative pathway of ethanol metabolism, namely the microsomal ethanol-oxidizing system. Indeed, this MEOS increases in activity after chronic ethanol consumption, with cross induction and acceleration of the metabolism of other drugs and increased lipoprotein production with hyperlipemia. There is also increased microsomal activation of hepatotoxic compounds (including drugs and possibly vitamin A). Fibrosis and cirrhosis can develop despite an associated adequate diet and even in the absence of alcoholic hepatitis. They are preceded by myofibroblasts and fibroblast proliferation. What eventually causes the increased number of myofibroblasts and promotes fibrosis is unclear, nor do we know the relative role of hepatocytes or mesenchymal cells in the process of fibroplasis. Possibly selective roles in this process of specific nutritional factors remain to be elucidated.
 ...
PMID:Alcohol, protein nutrition, and liver injury. 634 74

Antioxidant status was measured in heart, liver, kidney, lung, and erythrocytes of 2-week streptozotocin-diabetic male Wistar rats exposed to chronic intermittent psychological stress consisting of 1 h of restraint twice daily for 14 days. Diabetes reduced erythrocyte and heart and liver susceptibility to hydrogen peroxide-induced glutathione depletion. Susceptibility to peroxide-induced thiobarbituric acid reactive substance (TBARS) formation increased in erythrocytes, liver, kidney, and lung but decreased in heart. Significant changes also occurred in glutathione levels (increased in heart and decreased in liver) and in the activities of catalase (reduced in liver and kidney), glutathione reductase (elevated in heart and liver), and glutathione peroxidase (decreased in liver and lung), but not Cu,Zn-superoxide dismutase. Stress potentiated diabetes-associated hyperglycemia and attenuated diabetes-induced hyperlipidemia. In addition, the reduction in peroxide-induced glutathione depletion in heart and liver and the increased TBARS formation in kidney and lung were reversed. Similarly, the diabetes-induced induced increase in liver glutathione reductase and decreases in liver and lung glutathione peroxidase activities were abolished by stress. Thus, the relative resistance of antioxidant systems to stress can be modified under pathologic conditions in which antioxidant alterations are present.
 ...
PMID:Alteration of antioxidant status in diabetic rats by chronic exposure to psychological stressors. 857 2

1. We measured sodium-lithium countertransport, sodium-hydrogen exchange and membrane micro-viscosity in 48 individuals with familial hypercholesterolaemia, 33 subjects with hypertriglyceridaemia and 54 normolipaemic controls. Full lipid profile, blood pressure, body mass index, fasting glucose and insulin levels were also measured. 2. Subjects with hypertriglyceridaemia had higher blood pressure, body mass index, fasting glucose and insulin levels than normal controls. 3. Vmax of the sodium-lithium countertransport was elevated in the hypertriglyceridaemic group compared with controls. Across the whole group log(e) triacylglycerols correlated with Vmax of the sodium-lithium countertransport. There was no difference in sodium-lithium countertransport K(m) between the groups. 4. Sodium-hydrogen maximal proton efflux rate (Vmax) and K(m) were not different between the three groups. There were no correlations between sodium-hydrogen exchange and sodium-lithium countertransport parameters. 5. Microviscosity as measured by diphenylhexatriene was reduced at the core of the membrane in subjects with hypertriglyceridaemia compared with those with familial hypercholesterolaemia or normolipaemic controls, suggesting an alteration in membrane structure. 6. Changes in sodium transport in hyperlipidaemia may be mediated by changes in membrane structure resulting in altered protein conformation or turnover.
 ...
PMID:Sodium-lithium countertransport, sodium-hydrogen exchange and membrane microviscosity in patients with hyperlipidaemia. 909 3

Free radical activity may contribute to atherosclerotic lesions which in diabetic subjects may frequently lead to vascular complications. It is known that oxidative stress is associated to diabetes. Protein glycation and glucose oxidation could be possible source of free radicals. 28 non insulin dependent diabetic subjects (NIDDM) were examined. 20 healthy subjects matched for age, sex and for the presence of hypertension and hyperlipidemia were also studied. Hydrogen peroxide, measured by intracellular levels of the fluorescent 2,7-dichloro-fluorescein (DCF), was considered as indicative parameter of free radical production. The results showed that in resting platelets the basal level of hydrogen peroxide was significantly higher in diabetic subjects than in controls. Moreover, after stimulation with thrombin, collagen, phorbol myristate acetate (PMA) and platelet activating factor (PAF), platelets of diabetic subjects generated significantly higher amounts of hydrogen peroxide than controls. Moreover, platelet aggregation induced by adenosine 5'-diphosphate (ADP) and plasma beta TG levels were higher in diabetics than in controls. In diabetic patients platelet free radical production and functional activity are increased and therefore could play a role in the elevated thrombotic risk described in diabetes.
 ...
PMID:Hyperactivity and increased hydrogen peroxide formation in platelets of NIDDM patients. 917 36

Previous clinical studies reported elevated semicarbazide-sensitive amine oxidase (SSAO) activity in insulin-dependent diabetes mellitus (IDDM), but there are not sufficient data about SSAO in non-insulin-dependent diabetes mellitus (NIDDM). The present study was conducted to investigate serum SSAO activity in NIDDM patients compared with nondiabetic and IDDM patients. Serum SSAO activity in 61 patients with diabetes (n = 34 NIDDM and n = 27 IDDM) and 36 controls was determined using 14C-benzylamine as a substrate. NIDDM and IDDM patients exhibited higher SSAO activity compared with controls ([mean +/- SD] NIDDM, 164.60+/-69.43 pmol/mg protein/h, P<.0001; IDDM, 143.91+/-72.45 pmol/mg protein/h, P<.002; control, 91.46+/-28.11 pmol/mg protein/h). There was a significant positive correlation between serum SSAO activity and the body mass index (BMI), body weight, hemoglobin A1c (HbA1c), fasting plasma glucose, and triglycerides. Within the control group, SSAO correlated with total cholesterol levels. The progression and severity of diabetic complications such as angiopathy may be exacerbated by cytotoxic metabolites (e.g., formaldehyde and hydrogen peroxide) formed by SSAO. These results reveal the possibility that elevated serum SSAO activity in association with obesity and hyperlipidemia may be a cardiovascular risk factor in diabetes mellitus.
 ...
PMID:Elevated serum semicarbazide-sensitive amine oxidase activity in non-insulin-dependent diabetes mellitus: correlation with body mass index and serum triglyceride. 992 Jan 54

We have previously demonstrated that bradykinin blocks hypertrophy of isolated cardiomyocytes: this is dependent on the release of nitric oxide from endothelial cells. In the present study, we investigated the influence of endothelial dysfunction on the antihypertrophic action of bradykinin. Angiotensin II (1 microM) induced a 34 +/- 2% increase in [3H]phenylalanine incorporation (P<0.001), an in vitro marker of hypertrophy, in adult rat cardiomyocytes co-cultured with bovine aortic endothelial cells. This response was blocked by bradykinin (10 microM), but restored by the nitric oxide synthase inhibitor. N(omega)-monomethyl-L-arginine (100 microM). However, the antihypertrophic effect of bradykinin in co-culture was abolished by 24 h pretreatment of endothelial cells with high glucose (25 mM, to mimic hyperglycemia) and attenuated by hydrogen peroxide (100 microM, to mimic oxidative stress). Pretreatment with oxidized low-density lipoprotein (100 microg/ml for 24 h, to mimic hyperlipidemia) was without effect. The hypertrophic response to angiotensin II was not modified by endothelial cell pretreatment. Furthermore, the ability of bradykinin to elevate cGMP (a marker for nitric oxide) in cardiomyocytes co-cultured with endothelial cells was attenuated by pretreatment with either high glucose or hydrogen peroxide. In conclusion, loss of the cardioprotective action of bradykinin against angiotensin II-induced hypertrophy was associated with impaired nitric oxide release from dysfunctional endothelial cells.
 ...
PMID:Endothelial dysfunction limits the antihypertrophic action of bradykinin in rat cardiomyocytes. 1088 62

Tectorigenin and kaikasaponin III from the flowers of Pueraria thunbergiana showed potent hypoglycemic and hypolipidemic effects in the streptozotocin-induced diabetic rats. Intraperitoneal administration of these two compounds with 5 and 10 mg/kg, respectively, for seven days to streptozotocin-induced rats significantly reduced the blood glucose, total cholesterol, LDL- and VLDL-cholesterol and triglyceride levels when compared with those of control group. Glycitein in which 5-OH is unlinked and tectoridin (7-O-glycoside of tectorigenin) isolated from the flowers of P. thunbergiana did not improve hyperglycemia and hyperlipidemia. In addition, tectorigenin showed in vitro antioxidant effects on 1,1diphenyl-2-pirylhydrazyl (DPPH) radical, xanthine-xanthine oxidase superoxide anion radical, and lipid peroxidation in rat microsomes induced by enzymatic and non-enzymatic methods. We further found that tectorigenin and kaikasaponin III protected the Vero cell line (normal monkey kidney) from injury by hydrogen peroxide. From these findings, it seems likely that the antioxidant action of tectorigenin and kaikasaponin III may alleviate the streptozotocin-induced toxicity and contribute to hypoglycemic and hypolipidemic effects.
 ...
PMID:Hypoglycemic and hypolipidemic effects of tectorigenin and kaikasaponin III in the streptozotocin-lnduced diabetic rat and their antioxidant activity in vitro. 1105 24


1 2 3 4 5 Next >>