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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antioxidant efficacy of vitamin E on Perchloroethylene (PER) induced cytotoxicity has been studied in rats. Feeding PER to rats for 42 days using sesame oil as vehicle alters total protein and protein bound carbohydrate components in liver and kidney of experimental animals. Supplementation of vitamin E prevented the changes observed in total protein and protein bound carbohydrate components of PER administered rats. Histopathological studies also show the effectiveness of vitamin E on PER administered rats in protecting the cellular architecture of liver and kidney from PER induced cytotoxicity.
Mol Cell Biochem 1995 Mar 09
PMID:In vivo effect of vitamin E on serum and tissue glycoprotein levels in perchloroethylene induced cytotoxicity. 779 40

Ozone (5 mumol.min-1) inhibited the human erythrocyte membrane Na(+)-K+ ATPase (EC.3.6.1.39) activity in a time dependent manner. Inhibition was more pronounced for the first 5 min of ozone exposure in the directly ozone exposed membranes than in the membranes prepared from ozone exposed erythrocytes. However, Na(+)-K+ ATPase activities of both preparations were inhibited to the same extent (about 70%) at the end of 10 min ozone exposure. It was also determined that there was a close relationship between the decrease of enzyme activity and the increase in the thiobarbituric acid reactive substances in both types of preparations. Na(+)-K+ ATPase was inhibited by ozone even at the presence of vitamin E or vitamin C. However, the degree of the inhibitions and the amounts of thiobarbituric acid reactive products formed were smaller than the corresponding values found in the absence of these vitamins.
Biochem Mol Biol Int 1994 Aug
PMID:Effects of ozone on the activity of erythrocyte membrane Na(+)-K+ ATPase. 780 27

Haemolysis induced by a free radical initiator (4,4'azobis-(4-cyanovaleric acid) has been studied with transfusion blood. Azobis cyanovaleric acid caused an increase in haemolysis. The effect of alpha- and gamma-tocopherol, 2,2,5,7,8 pentamethyl-6-chromanol and 2,2,7,8 tetramethyl-6-chromanol on the red blood cell haemolysis was studied. There was little difference in the antioxidant action of four chromanols studied. Compounds without the side chain appeared to suppress haemolysis as well as alpha- and gamma-tocopherol. These results suggest that the long side chain of vitamin E has little or no effect on its antioxidant activity in red blood cells. However "protection against haemolysis" was related to total chromanol content of red blood cells. Therefore by dividing "protection" by "total chromanol content" it can be seen that alpha-tocopherol has the highest antioxidant potency.
Biochem Mol Biol Int 1994 Aug
PMID:Oxidation of human red blood cells by a free radical initiator and effects of radical scavengers. 780 42

Experimental work in our laboratory has confirmed the protective activity of vanadium compounds on hyperglycemia and glycosuria in streptozotocin (STZ) diabetes. Furthermore, diabetic cataract has also been partially prevented. Nevertheless, the combination of a natural antioxidant, vitamin E, with Na3 VO4 has not further enhanced this ameliorating effect. Our experimental approach has been an attempt to block the prooxidant activity of both STZ and vanadate, with the purpose of eliciting the best possible antidiabetic protection. More recently, a lipid soluble synthetic antioxidant U-78517F, a 2-methylaminochroman, has been reported to have a significant protective effect against brain injury and ischemia. This compound inhibits the iron-dependent lipid peroxidation 100 times more effectively than vitamin E. This investigation has introduced a combination of the vanadium compound plus the aforesaid lazaroid, as its (-) enantiomer, U-83836E, in order to improve the insufficient protection when vitamin E was used. For twelve weeks, male Wistar rats, rendered diabetic with STZ, were administered Na3VO4 in drinking water along with the lazaroid carried by the food. Four, eight and twelve weeks after the beginning of the protective treatment, fluid and food intake, diuresis and excreted feces, glycosuria and proteinuria were determined on biological samples obtained in metabolic cages; body weight and glycemia were also recorded. At weeks 6 and 12 of the treatment, the opaqueness of the eye lenses was controlled and registered. At the end of the experiment, circulating glycosylated hemoglobin (HbA1c), fructosamine, N-acetyl-beta-D-glucosaminidase (NAG), and fluorescent peroxides were evaluated. Within the first month of treatment, protection by the combination paralleled that elicited by vanadate alone. At subsequent steps, U-83836E significantly improved the protective effect of vanadate alone on polydipsia and polyuria, but especially on hyperglycemia and glycosuria. The further ameliorating effect of the lazaroid was also observed on HbA1c and NAG, and, most important, on the cataract. In conclusion, these findings demonstrate that the lazaroid U-83836E succeeds in further protecting the most important symptoms of diabetes treated with vanadate, and that this antioxidant acts effectively even when it is administered orally in food, in a non invasive manner.
Res Commun Mol Pathol Pharmacol 1994 Sep
PMID:Amelioration of diabetes and cataract by Na3VO4 plus U-83836E in streptozotocin treated rats. 782 6

The effect of dietary vitamin E supplementation upon macrophage metabolism and function was examined in aged rats fed a balanced or a polyunsaturated-rich diet. The following parameters were studied: number of cells in the intraperitoneal cavity, maximal activity of hexokinase, citrate synthase, glucose-6-phosphate dehydrogenase, glutathione peroxidase and phosphate-dependent glutaminase. The consumption of glucose and the production of lactate, hydrogen peroxide and thiobarbituric reactive substances were measured in control ONCO-BCG injected rats. The results indicated that vitamin E has no significant effect on the values of the parameters studied in the macrophages of rats fed a balanced diet both for 3 (mature) or 17 months (aged). This antioxidant did not provoke any response on the changes caused by ageing the animals. However, several of the metabolic and functional alterations in macrophage induced by the polyunsaturated-rich diets were reversed by the inclusion of vitamin E in the diet. These changes were associated with macrophage migration capacity, citrate synthase and glucose-6-phosphate dehydrogenase activities and the content of lipid peroxides. The findings suggest that vitamin E has a beneficial effect for macrophage metabolism and function, but the effects are confined to particular circumstances.
Biochem Mol Biol Int 1994 Aug
PMID:Effect of dietary vitamin E supplementation on macrophage metabolism during ageing. Study in rats fed fat-rich diets during ageing. 784 17

We investigated the association between vitamin E, lipid peroxidation and eicosanoid production in experimental alcoholic liver injury. We used the intragastric feeding rat model in which animals were fed corn oil and ethanol (CO+E) and corn oil and dextrose (CO+D) for 2 and 4 week periods. At sacrifice, we measured plasma levels of alpha-tocopherol, 8-isoprostane, thromboxane B2 (TXB2) and 6-ketoprostaglandin F1 alpha (6-KetoPGF1 alpha). Animals fed CO+E had significantly lower concentrations of alpha-tocopherol and higher concentrations of 8 isoprostane at both 2 and 4 weeks. a significant inverse correlation was seen between alpha-tocopherol concentrations and the TXB2: PGF1 alpha ratio (r = 0.72, p < 0.01). A positive correlation was seen between the TXB2: PGF1 alpha ratio and 8 isoprostane levels (r = 0.84, p < 0.001). These results suggest that vitamin E depletion and enhanced lipid peroxidation may affect eicosanoid metabolism in experimental alcoholic liver disease in such a way so as to increase the thromboxane to prostacyclin ration.
Mol Cell Biochem 1994 Nov 09
PMID:Eicosanoid production in experimental alcoholic liver disease is related to vitamin E levels and lipid peroxidation. 787 2

The anticarcinogenic activity of alpha-tocopherol (Vitamin E) was tried in fibrosarcoma induced rats through its antioxidative potential. The rate of formation of malondialdehyde (MDA), the end product of lipid peroxidation was analysed in alpha-tocopherol (400 mg/kg body weight) treated and untreated fibrosarcoma bearing rats with respective controls. The levels of non-enzymic antioxidants like, glutathione and vitamin E, and enzymic antioxidants viz., catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), and glutathione-S-transferase (GST) were assayed as well. Significantly increased (p < 0.001) level of lipid peroxide was observed with concomitant decreases in the level of enzymic and non-enzymic antioxidants in fibrosarcoma bearing rats when compared with control animals. In alpha-tocopherol supplemented animals, the corrected level of these parameters were observed likely to near normal values. Thus, alpha-tocopherol can be accepted to pose first line of defense mechanism against excessively formed reactive species due to impaired antioxidant systems in fibrosarcoma conditions, that cause membrane damage leading to deleterious effects.
Mol Cell Biochem 1994 Feb 23
PMID:Effect of alpha-tocopherol on lipid peroxidation and antioxidant system in fibrosarcoma bearing rats. 803 77

We have studied the effect of Mg deficiency on both tissue mineral content and liver oxidative status. Male Wistar rats kept for eight weeks on a Mg-deficient diet (Mg 152ppm) quickly developed a severe plasma Mg deficiency (73% decrease). The content of Cu and Fe significantly increased in different tissues following the treatment. Liver glutathione, CuZn-superoxide dismutase, and vitamin E were significantly reduced (by about 16%, 18% and 30% respectively). Lipid peroxidation, induced in vitro by NADPH/ADP-Fe3+ and measured as MDA formation, increased by about 100% after 20 min incubation in liver microsomes isolated from Mg-deprived rats. The alterations found in the content of transition metals and in the level of both cytosolic and membrane antioxidants, as well as the higher sensitivity of liver microsomes to lipid peroxidation in vitro, are consistent with an oxidative stress occurring in vivo in the tissues of Mg-deficient animals.
Biochem Mol Biol Int 1994 Apr
PMID:Mg deficiency induces mineral content changes and oxidative stress in rats. 806 40

The effects of age and hypertension on the antioxidant defence systems and the lipid peroxidation in rat isolated hepatocytes were studied. Four different age groups (1, 3, 6 and 12 months) were considered in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. Age-associated changes were observed on vitamin E status, glutathione (GSH) level, MDA formation and glutathione peroxidase (GSH-Px) activity in both strains. Maximal levels or activities of these parameters were found at 3 and 6 months, except for MDA which was low at 3 months. Then, a fall was observed at 12-month-old compared to 6-month values. In addition, GSH-Px activity was significantly lower in SHR than in WKY rats, except at the age of one month. The decrease of this enzyme activity could induce an increased cellular generation of radical species and lipid peroxidation, which might be link to hypertension.
Mol Cell Biochem 1994 Mar 16
PMID:Age-related changes in antioxidant defence mechanisms and peroxidation in isolated hepatocytes from spontaneously hypertensive and normotensive rats. 807 5

Familial hypobetalipoproteinemia is caused by apolipoprotein (apo) B gene mutations and is frequently associated with a truncated apo-B protein in the plasma. Homozygosity for mutations yielding a truncated apo-B is extremely rare; fewer than five true homozygotes have been described in the world's literature. These patients typically have normal levels of triglycerides and virtually absent low density lipoprotein (LDL) cholesterol. The clinical status of these patients is variable, ranging from asymptomatic in two homozygotes who synthesized a truncated apo-B (apo-B87) to severe neurological disease resulting from vitamin E deficiency in a homozygote who synthesized a shorter apo-B (apo-B50). In this report, we describe a 48-year-old female homozygous for a nonsense mutation resulting in an even shorter apo-B, apo-B45.2. Although this individual had virtually no LDL cholesterol, she was asymptomatic and had normal plasma levels of vitamin E. This case demonstrates that homozygosity for an apo-B mutation associated with a relatively short apo-B truncation can be completely asymptomatic.
Hum Mol Genet 1994 May
PMID:Asymptomatic homozygous hypobetalipoproteinemia associated with apolipoprotein B45.2. 808 60


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