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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.
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PMID:Determination of uric acid on continuous-flow (AutoAnalyzer II and SMA) systems with a uricase/phenol/4-aminophenazone color test. 62 57

An improved method for analysis of serum iron is described which is simple, rapid, precise and convenient for routine use in clinical laboratories. Serum proteins are precipitated with trichloroacetic acid-hydrochloric acid solution, with simultaneous release of Fe(III) from transferrin. Fe(III) is reduced to Fe(II) by sodium ascorbate, and Fe(II) is reacted with ferrozine to form a lavender complex, which is measured by spectrophotometry at 562 nm. Measurements of iron in 183 serum samples by this method were compared with measurements by a "direct" spectrophotometric method without without deproteinization, as previously described. Close agreement was obtained in 171 of these 183 pairs of analyses (93.5 percent). Discrepancies (greater than 12 mug per dl) were noted in the remaining 12 serums, which were attributed to interference in direct spectrophotometric analyses of iron, owing to (1) hemolysis, (2) lipemia, (3) jaundice, (4) protracted storage or (5) repeated freezing and thawing of the serums.
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PMID:Modified method for analysis of serum iron. 116 95

The aim of the study was to establish whether it is possible, in a group of deliberately selected subjects with hyperlipidaemia, to modulate cholesterol levels by ascorbic acid administered at a dose of 500 mg/day. The authors assessed the levels of vitamin C, total and HDL cholesterol, triacylglycerols in the blood serum of 140 probands assigned to an 83-member experimental group, and to a 57-member control group. The experimental group was provided Celaskon effervescens Spofa at a dose of 500 mg/day/person. The experiment lasted for 18 months. Blood collections were made in the whole cohort at six-month intervals. Administration of L-ascorbic acid led to a highly significant decrease in the levels of total and LDL cholesterol. After 12 months of study, a highly significant decrease in atherogenic index and an increase in HDL cholesterol levels were found persisting until the end of the experiment.
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PMID:Plasma lipids, lipoproteins and atherogenic index in men and women administered vitamin C. 130 21

Chronic vitamin C deficiency was induced in guinea pigs by restricting their vitamin C intake to 0.5 mg daily. This was just sufficient to prevent rapidly fatal scurvy and 55 per cent of the animals survived. In 16 weeks their serum ascorbic acid (SAA) fell to 0.16 +/- 0.06 mg/dl as compared to 0.73 +/- 0.11 in control animals receiving 5 mg vitamin C daily. There was a marked increase in serum cholesterol, LDL-cholesterol, VLDL-cholesterol, triglycerides and total lipids. HDL-cholesterol was, however, decreased resulting in a shift of the LDL/HDL ratio from 1.13 +/- 0.16 in the control to 5.91 +/- 1.70 in the low vitamin C group. Cholesterol feeding (100 mg/day) by itself lowered the SAA significantly, besides producing hyperlipidemia. When the vitamin C intake was reduced to only 0.5 mg/day, the effects of cholesterol feeding were exaggerated; the magnitude of hyperlipidemia was now significantly greater than with simple cholesterol feeding. The LDL/HDL ratio rose to 19.02 +/- 3.32 from 1.13 +/- 0.16 in the normal guinea pigs. Chronic vitamin C deficiency seems to affect the blood lipid profile unfavourably which could promote atherogenesis.
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PMID:Aggravation of cholesterol induced hyperlipidemia by chronic vitamin C deficiency: experimental study in guinea pigs. 325 10

Vitamins are a group of organic compounds occurring naturally in food and are necessary for good health. Lack of a vitamin may lead to a specific deficiency syndrome, which may be primary (due to inadequate diet) or secondary (due to malabsorption or to increased metabolic need), and it is rational to use high-dose vitamin supplementation in situations where these clinical conditions exist. However, pharmacological doses of vitamins are claimed to be of value in a wide variety of conditions which have no, or only a superficial, resemblance to the classic vitamin deficiency syndromes. The enormous literature on which these claims are based consists mainly of uncontrolled clinical trials or anecdotal reports. Only a few studies have made use of the techniques of randomisation and double-blinding. Evidence from such studies reveals a beneficial therapeutic effect of vitamin E in intermittent claudication and fibrocystic breast disease and of vitamin C in pressure sores, but the use of vitamin A in acne vulgaris, vitamin E in angina pectoris, hyperlipidaemia and enhancement of athletic capacity, of vitamin C in advanced cancer, and niacin in schizophrenia has been rejected. Evidence is conflicting or inconclusive as to the use of vitamin C in the common cold, asthma and enhancement of athletic capacity, of pantothenic acid in osteoarthritis, and folic acid (folacin) in neural tube defects. Most of the vitamins have been reported to cause adverse effects when ingested in excessive doses. It is therefore worthwhile to consider the risk-benefit ratio before embarking upon the use of high-dose vitamin supplementation for disorders were proof of efficacy is lacking.
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PMID:Vitamin therapy in the absence of obvious deficiency. What is the evidence? 623 Feb 19

Effects of L-ascorbate 2-sulfate (AAS) on fatty liver and hyperlipidemia induced by various treatments were studied in rats and guinea pigs. L-Ascorbic acid (AA) (50 or 175 mg/kg), a reference compound, lowered the lipid levels in the serum and/or liver in guinea pigs, while AA had little effect in rats. On the other hand, AAS (300 mg/kg) was effective in both animals. In rats, AAS lowered cholesterol and triglycerides in the serum from ethionine-treated animals and in the liver from orotic acid-supplemented animals. In guinea pigs, this compound lowered cholesterol and triglycerides in the serum from ethionine-treated animals, lipids in the liver from cholesterol-supplemented animals, and lipids in the serum and liver from scorbutic animals. AA markedly increased the content of AA in the organs in all experiments, while AAS had a slight effect. Thus, it is suggested that AAS exerts its hypolipidemic and lipotropic effects by the specific actions of AAS.
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PMID:Effect of l-ascorbate 2-sulfate on fatty liver and hyperlipidemia induced by various treatments in rats and guinea pigs. 724 Dec 35

The most consistent toxic effects of dioxin-type chemicals are hyperlipidemia, body weight loss (particularly body fat loss), anorexia, changes in carbohydrate metabolism, and lipid peroxidation. The biochemical systems particularly affected are lipoprotein lipases, low-density-lipoprotein receptors, glucose transporter proteins (GLUTs), vitamin C uptake, and insulin secretion. Some of these biochemical changes occur at very low doses, and some effects can last for long time periods. To provide a mechanistic explanation for such actions of dioxins, available experimental evidence has been reviewed. The most recent discovery indicates that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) directly acts with isolated cytosolic aryl-hydrocarbon (Ah) receptor under cell-free conditions even without the presence of the nucleus and is capable of activating key protein kinases that are involved in the growth factor signal-transduction pathway. The resulting activation of primary-response transcription factors in the nucleus appears to play a key role in coordinating vital cell program shifts, including lipid metabolism.
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PMID:Mechanism of action of dioxin-type chemicals, pesticides, and other xenobiotics affecting nutritional indexes. 787 40

We report an impressive decline in plasma lipid resistance to oxidation during Triton-WR-1339-induced hyperlipidemia in rats. This decline is associated with a modification in the balances between alpha-tocopherol and lipids and alpha-tocopherol and ascorbate. These results are consistent with a weak resistance of accumulated native lipoproteins in plasma to oxidation, during a 6-hour time course, and they suggest a misunderstood role of lipoprotein catabolic enzymes: to improve this characteristic. Conclusively, the results lead us to propound Triton-induced hyperlipidemia as an original model for studying the balance impairment between antioxidants and oxidizable substrates.
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PMID:Weak resistance to oxidation of native lipoproteins in Wistar rats. 851 35

The effect of vitamin C supplementation on hepatic cytochrome P450 expression was investigated in streptozotocin (STZ) diabetic male Wistar Albino rats. STZ-treated rats displayed the usual characteristics of diabetes including; hyperphagia, polydipsia, decreased body weight gain and also the increased expression and activity of hepatic CYP1A, 2B, 2E and 4A proteins. Vitamin C administration in drinking water (2% w/v) was associated with significant decreases in the levels of hyperglycaemia (P < 0.05), glycosylated haemoglobin (P < 0.05), hyperlipidaemia (P < 0.001), and hyperketonaemia (P < 0.001) associated with STZ-diabetes. Vitamin C-treatment selectively reduced the activity and expression of CYP2E proteins (P < 0.001). These effects on CYP2E expression may be mediated by the reduced levels of circulating ketone bodies, however, a direct effect on CYP2E expression in diabetes cannot be discounted.
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PMID:Effect of vitamin C supplementation on hepatic cytochrome P450 mixed-function oxidase activity in streptozotocin-diabetic rats. 900 94

The present study was to investigate the levels of plasma lipid peroxide products including malondialdehyde (MDA) and conjugated dienes (CD), and antioxidants including enzyme superoxide dismutase, glutathione peroxidase, catalase, plasma vitamin E and vitamin C in diabetic patients. Fifty-eight diabetic subjects; 16 males and 42 females, aged 30-75 years, were recruited. Eighteen of them had diabetes and forty of them had diabetes with hyperlipidemia. Twenty-seven healthy subjects, 8 males and 19 females, aged 30-75 years, were used as the control group. The results showed that the concentrations of plasma MDA in diabetic patients with or without hyperlipidemia tended to be increased when compared to the controls but there were no significant differences. The CD values were increased significantly in both diabetic groups when compared with control subjects. Significantly elevated levels of plasma MDA and CD were found in diabetic patients with hypertriglyceridemia (> 150 mg%). This increment did not change the antioxidant status in both enzymes and vitamins except that the plasma vitamin E levels and the ratios of tocopherol: cholesterol were increased significantly. An increase of lipid peroxide in plasma may be one important factor in the development of vascular complication and atherosclerosis seen in diabetic patients.
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PMID:Plasma lipid peroxide and antioxidant levels in diabetic patients. 924 11


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