Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:EXPT03226 (vitamin E)
 17,558 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In two experiments the effect of feeding dried crushed white and red grape press cake replacing 10--20% of the complex feed mixture A1 and SOL, was studied on the 21 biochemical indicators of blood serum, plasma, suprarenal glands, liver and tissue of fattened pigs. Changes indicating unsuitability of this non-traditional feed were not observed. During feeding red grape press cake, the young pigs of 35kg body weight had a lower concentration of glucose in blood serum, in comparison with the control. The temporary increase of calcium level and decrease of inorganic phosphorus in these animals was accompanied by a lower activity of alkaline phosphatase. White and red grape press cake affected positively the vitamin E level in blood serum. In the muscles of the experimental slaughter pigs protein proportion was increased and fat proportion was decreased.
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PMID:[Changes in biochemical indicators in the blood and organs of pigs fed dried grape press cake]. 11 74

Weanling rats were fed vitamin E deficient diets for 6 to 15 weeks and then given vitamin E orally for 4 days. Plasma obtained 1 day after the last dose was assayed for glutamic oxalacetic transaminase (GOT) and pyruvate kinase activity (PK). Administration of vitamin E resulted in reduction in activity of both enzymes. Plasma levels of alkaline phosphatase, lactic dehydrogenase, and bilirubin were unaffected by vitamin E and there was no histological evidence of liver degeneration. The number of phagocytized muscle fibers was greatly reduced by vitamin E treatment, but a substantial number of necrotic fibers were still present. With more prolonged (8 days) treatment, plasma PK and GOT levels were reduced to levels found in plasma of vitamin E replete animals and few degenerated muscle fibers could be observed. It was concluded that resolution of the necrotizing myopathy in vitamin E deficient rats is a rapid process and that the decreased activity of PK and GOT in plasma is a sensitive indicator of the resolution process. The decrease in plasma enzyme levels is an easily quantitated and reproducible biological response to vitamin E administration. Thus, this approach provides a basis for a sensitive and accurate bioassay for vitamin E activity.
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PMID:Plasma activity of pyruvate kinase and glutamic oxalacetic transaminase as indices of myopathy in the vitamin E deficient rat. 72 46

The paper described the findings of the activity of aspartate amino transferase (GOT) and alanine amino transferase (GPT), lactate dehydrogenase (LDH), alkaline phosphatase (AP), and aldolase in the blood serum of calves examined for white-muscle disease (WMD). Relapsing mass accurrence of the disease was reported from various agricultural enterprises where calves were fed a milk replacer without vitamin E. In comparison with clinically healthy calves fed a feed mixture with vitamin E, calves suffering from the clinical form of WMD showed an alkaline phosphatase level decrease from 32.3 +/- 7.6 u. K. A. to 15.1 +/- 8.2 u. K. A. On the other hand, the activites of ALD, GOT, GPT, and LDH showed a statistically significant increase. The acute and sub-acute course of the disease increased enzyme activities as follows: ALD from 4.2 +/- 1.1 mumol (= 70.0 +/- 17.0 i.u.) to 9.7 +/- 2.1 mumol (= 163.0 +/- 33.2 i. u.), GOT from 0.9 +/-0.5 mumol (= 68.0 +/- 5.8 i.u.) to 16.7 +/- 11.7 mumol (= 567.0 +/-40.0 i. u.) GPT from 0.2 +/- 0.8 mumol (= 5.0 +/- 12.4 i. u.) to 9.8 +/- 2.8 mumol (= 330.0 +/- 40.4 i.u.), LDH from 46.1 +/- 5.4 mumol (= 765.0 +/- 40.0 i.u.) to 72.7 +/- 24.3 mumol (= 1,207.0 +/- 403.0 i.u.). In WMD-affected herds, similar enzyme activity fluctuations were observed even in calves showing no clinical signs of the disease. It follows from the study that the examination of serum enzymes provides a method to demonstrate the clinical and pre-clinical forms of white-muscle disease and that it can be included in the set of tests for the diagnosis of diseases in calves. The significant differences in all calves in the affected herds show that the disease is a danger to all animals in the herd fed a deficient mixture.
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PMID:[Activity of some serum enzymes in calves suffering from white muscle disease]. 81 57

The paper described the findings of the activity of aspartate amino transferase (GOT) and alanine amino transferase (GPT), lactate dehydrogenase (LDH), alkaline phosphatase (AP), and aldolase in the blood serum of calves examined for white-muscle disease (WMD). Relapsing mass accurrence of the disease was reported from various agricultural enterprises where calves were fed a milk replacer without vitamin E. In comparison with clinically healthy calves fed a feed mixture with vitamin E, calves suffering from the clinical form of WMD showed an alkaline phosphatase level decrease from 32.3 +/- 7.6 u. K. A. to 15.1 +/- 8.2 U. K. A. On the other hand, the activities of ALD, GOT, GPT, and LDH showed a statistically significant increase. The acute and subacute course of the disease increased enzyme activities as follows: ALD from 4.2 +/- 1.1 mumol (= 70.0 +/- 17.0 i. u.) to 9.7 +/- 2.1 mumol (= 163.0 +/- 33.2 i. u.), GOT from 0.9 +/- 0.5 mumol (= 68.0 +/- 5.8 i. u.) to 16.7 +/- 11.7 mumol (= 567.0 +/- 40.0 i. u.), GPT from 0.2 +/- 0.8 mumol (= 5.0 +/- 12.4 i. u.) to 9.8 +/- 2.8 mumol (= 330.0 +/- 40.4 i. u.), LDH from 46.1 +/- 5.4 mumol (= 765.0 +/- 40.0 i. u.) to 72.7 +/- 24.3 mumol (= 1,207.0 +/- 403.0 i. u.). In WMD-affected herds, similar enzyme activity fluctuations were observed even in calves showing no clinical signs of the disease. It follows from the study that the examination of serum enzymes provides a method to demonstrate the clinical and pre-clinical forms of white-muscle disease and that it can be included in the set of tests for the diagnosis of diseases in calves. The significant differences in all calves in the affected herds show that the disease is a danger to all animals in the herd fed a deficient mixture.
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PMID:[Activity of various serum enzymes in calves suffering from nutritionally-induced muscular dystrophy]. 81 73

12-Keto oleic acid, possibly one of the oxidation products of long-chain, unsaturated fatty acids, was added to the feed of weanling male rats at the 1% level. Their growth curves, tissue weights, plasma alkaline phosphatase, GOT, and GPT activities, and plasma and liver lipid (cholesterol, triglyceride and phospholipid) levels were investigated and compared with those of weanlings fed a vitamin E deficient diet. Both the diet containing 12-keto oleic acid and the diet deficient in vitamin E decreased the growth rate of body weight and tissue weight, and increased the liver triglyceride and cholesterol levels. Parallel with these, increased hemolysis and stimulation of lipid peroxidation and fluorescent production in the liver homogenate were observed. Elevated plasma alkaline phosphatase and GOT activities which may be considered to be due to a functional disorder of the liver were also observed.
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PMID:Exacerbating effect of dietary 12-keto oleic acid on vitamin E deficiency in the rat. 115 7

The influence of vitamin E on cadmium intoxication was investigated in rats. The exposure to cadmium (1 mg/kg, Cd as CdCl2.2H2O, intraperitoneally for 7 days) decreased the activity of hepatic and renal glutamic oxalacetic and glutamic pyruvic transaminases (GOT, GPT) and alkaline phosphatase (ALP) accompanied by increase in the levels of serum GOT and GPT and urinary protein. Simultaneous administration of vitamin E (5 mg/kg, intramuscularly for 7 days) reduced these Cd induced biochemical alterations. The accumulation of Cd in blood, liver and kidney also decreased significantly upon co-exposure to vitamin E. The antioxidant property of vitamin E seems to be responsible for the observed protection of Cd intoxication.
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PMID:Preventive effect of vitamin E in cadmium intoxication. 158 65

Blood vitamin (thiamin, riboflavin, vitamins B6, B12, C, A, and E, folate and beta-carotene), mineral (iron and zinc), alkaline phosphatase and cholesterol levels and hematocrit were assessed in 960 school-age children selected by random sampling from urban and rural regions of Turkey. Nutritional statuses of the children according to each index were compared with respect to age, sex, area and type of settlement. A biochemical deficiency was observed in 20.1% of the children for thiamin, in 89.9% for riboflavin, in 83.4% for vitamin B6, in 23.3% for folate, in 5.9% for vitamin B12, in 43.0% for vitamin C, in 11.6% for vitamin A, in 3.5% for beta-carotene, in 21.8% for vitamin E, in 6.1% for iron, and in 15.7% for zinc. Hematocrit was low in 54.3%. Alkaline phosphatase and cholesterol levels were found to be above normal in 54.6% and 4.9% of the children respectively. It is surmised that a major cause of the deficiencies was an ignorance of good dietary practice. Although the children were found to be relatively short according to the National Center for Health Statistics standards, their normalised weights were within acceptable limits, which suggested a prevalence of stunting but not wasting in this population.
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PMID:Blood vitamin and mineral levels in 7-17 years old Turkish children. 158 3

To assess whether lipid peroxidation of hepatic mitochondria is associated with cholestatic hepatic injury we examined the effect of bile duct ligation (BDL) versus sham surgery on mitochondrial lipids of rats maintained on one of seven diets. Diets included vitamin E-deficient (E-) and vitamin E-sufficient (E+) combined with normal lipid (11.9% calories as stripped corn oil), high lipid (35% calories as stripped corn oil), or n-3 fatty acid (fish oil) supplementation. Rats were killed 17 days after surgery, mitochondria were isolated by differential centrifugation, and lipid-conjugated dienes and thiobarbituric acid-reacting substances (TBARS) were measured in mitochondrial lipids as indices of lipid peroxidation. BDL resulted in significant increases in lipid peroxidation in all dietary groups. The E- high lipid diets (with either corn oil or fish oil) were associated with higher lipid peroxide and serum bilirubin values in BDL rats compared to the normal lipid diets. Fish oil supplementation did not ameliorate cholestatic or oxidative injury. Serum alanine aminotransferase, bilirubin, alkaline phosphatase, and cholylglycine levels correlated significantly with levels of mitochondrial conjugated dienes and TBARS. These data suggest that free radical stress occurs during BDL in the rat and may result in mitochondrial lipid peroxidation, and that diets high in lipid may increase free radical damage to hepatic mitochondria. The role of free radicals in cholestatic hepatic injury requires further investigation.
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PMID:Effect of dietary lipid and vitamin E on mitochondrial lipid peroxidation and hepatic injury in the bile duct-ligated rat. 177 Mar 17

1. The sequence of renal cellular membrane damage induced by gentamicin was studied in the rat by using the release of alkaline phosphatase, acid phosphatase, muramidase and protein from renal cells as indices of renal damage. 2. The protective effect of a combination of vitamin E and selenium against renal damage was also investigated. 3. Gentamicin (60 mg kg-1 body weight) was nephrotoxic within 12 h of the first dose. 4. The plasma membrane of the renal tubules is damaged before the lysosomal membrane is affected. 5. A combination of vitamin E (1 mg g-1 body weight) and selenium (4 x 10(-3) mg g-1 body weight) attenuates the renal damage induced by gentamicin. Results suggest synergism between vitamin E and selenium in attenuating the renal damage. The possible mechanism of attenuation is discussed. 6. Vitamin E and selenium may have anti-diuretic potential.
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PMID:Vitamin E and selenium in gentamicin nephrotoxicity. 226 Dec 41

We studied intestinal absorption of vitamin E in 26 adults with primary biliary cirrhosis (PBC) and 6 control subjects. Seven (27%) PBC patients were vitamin E-deficient based on the ratio of serum vitamin E to serum total lipid concentrations. An oral vitamin E tolerance test was performed in all patients and control subjects using a loading dose of 2000 IU alpha-tocopheryl acetate with measurement of serial serum vitamin E concentrations over 24 h. Vitamin E absorption was expressed as the maximal rise in serum vitamin E above baseline, the area under the oral tolerance test curve, and these two values divided by the fasting total serum lipid concentration. Absorption of vitamin E was significantly impaired in all PBC patients vs. control subjects (p less than 0.01), in vitamin E-deficient vs. vitamin E-sufficient PBC patients (p less than 0.05 to p less than 0.01), and in PBC patients with serum vitamin E levels below 10 micrograms/ml vs. those with serum vitamin E levels above 10 micrograms/ml (p less than 0.01). Vitamin E absorption was inversely related to stage of PBC, serum cholylglycine, total bilirubin, cholesterol, alkaline phosphatase, aspartate aminotransferase, and prothrombin time. Patients with serum vitamin E below 10 micrograms/ml, serum total bilirubin above 3 mg/dl, serum cholylglycine above 600 micrograms/dl, or serum alkaline phosphatase above 1000 IU/L had severe malabsorption of vitamin E and would be at high risk for the development of vitamin E deficiency. Therefore, vitamin E supplementation should be considered not only in patients in whom overt vitamin E deficiency is present, but also in PBC patients meeting these criteria.
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PMID:Intestinal malabsorption of vitamin E in primary biliary cirrhosis. 291 Jul 63


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