Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the effect of choice feeding two diets with different selenium (Se) content to young and old moderately Se-deficient laying hens on serum Se (SSe), glutathione peroxidase (GPX), vitamin E, creatine kinase (CK), aspartate aminotransferase (ASAT), thyroxine (T4) and triiodothyronine (T3). Each of two consecutive study parts (I and II) with the same hens and treatments began with a 6-week baseline period (Medium-Se diet), followed by a 9-week depletion period (Low-Se or Medium-Se diet), followed by a 6-week choice period with two different diets offered simultaneously (Medium-Se/Low-Se, Medium-Se/High-Se, or Low-Se/High-Se). During both depletion periods, SSe and GPX gradually decreased, whereas T4 gradually increased in hens fed Low-Se confirming gradual Se-depletion. T3 decreased transiently in young hens only. As reported earlier, Se-deficient hens preferred High-Se over Low-Se diet during the first 3 weeks of choice feeding in part I, not however in part II. This preference resulted in higher SSe in these hens. GPX activity did not reflect feed preference, probably because Se-intake exceeded Se-requirement for maximal GPX activity. In Part II, hens depleted with Low-Se diet had higher SSe when previously offered High-Se diet in either combination, than when offered Low-Se/Medium-Se, presumably due to Se-stores built during choice feeding in part I, which possibly prevented development of Se-deficiency in part II. In addition, in older hens, Se depletion proceeded faster, whereas Se-repletion by choice feeding was slower than in young hens, indicating the increase in Se requirement with advancing age. Vitamin E, ASAT and CK remained largely unchanged by the treatments.
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PMID:Effects of selenium depletion and selenium repletion by choice feeding on selenium status of young and old laying hens. 1637 89

Naringenin is a naturally occurring citrus flavanone, which has been reported to have a wide range of pharmacological properties. The present work was carried out to evaluate the effect of naringenin on antioxidant and lipid peroxidation status in liver of oxytetracycline-intoxicated rats. Intraperitonial administration of oxytetracycline 200 mg/kg for 15 days resulted a significant elevation in serum hepatospecific markers such as aspartate transaminase, alanine transaminase, alkaline phosphatase, lactate dehydrogenase, and bilirubin and the levels of lipid peroxidation markers (thiobarbituric acid reactive substances (TBARS) and lipid hydroperoxides) in liver. Oxytetracycline also caused a significant reduction in the activities of superoxide dismutase, catalase, glutathione peroxidase, reduced glutathione (GSH), vitamin C and vitamin E in liver. Oral administration of naringenin (50 mg/kg b.w.t.) with oxytetracycline significantly decreased the activities of serum aspartate transaminase, alanine transaminase, alkaline phosphatase, lactate dehydrogenase and the levels of bilirubin along with significant decrease in the levels of lipid peroxidation markers in the liver. In addition, naringenin significantly increased the activities of superoxide dismutase, catalase and GSH peroxidase as well as the level of GSH, vitamin C and vitamin E in liver of the oxytetracycline-treated rats. Our results demonstrate that naringenin exhibited antioxidant property and decrease the lipid peroxidation against oxytetracycline-induced oxidative stress in liver.
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PMID:Influence of naringenin on oxytetracycline mediated oxidative damage in rat liver. 1663 3

Monosodium glutamate (MSG) continues to function as a flavor enhancer in West African and Asian diets. The present study examines the modulatory effects of dietary antioxidant vitamin C (VIT C), vitamin E (VIT E) and quercetin on MSG-induced oxidative damage in the liver, kidney and brain of rats. In addition, the effect of these antioxidants on the possible genotoxicity of MSG was investigated in a rat bone marrow micronuclei model. MSG administered intraperitoneally at a dose of 4 mg/g body wt markedly increase malondialdehyde (MDA) formation in the liver, the kidney and brain of rats. Simultaneous administration of VIT C, VIT E and quercetin to MSG-treated rats significantly reduced this increase in MDA induced by MSG. VIT E reduced lipid peroxidation most in the liver followed by VIT C and then quercetin, while VIT C and quercetin showed a greater ability to protect the brain from membrane damage than VIT E. The decreased glutathione (GSH) level elicited by MSG in the three organs corresponded with marked increase in the activity of glutathione-S-transferase (GST). While MSG increased (P < 0.001) the activities of superoxide dismutase and catalase in the liver, it decreased significantly the activities of these enzymes in the kidney and the brain. The three antioxidants were effective at ameliorating the effects of MSG on GSH levels and the enzymes in the three organs examined. While MSG increased the activity of glucose-6-phosphatase in the liver and kidneys of rats (P < 0.001), the activity of the enzyme was abysmally low in the brain. There were marked increases in the activities of alanine aminotransferase, aspartate aminotransferase and gamma-glutamyl transferase in rats treated with MSG. The antioxidants tested protected against MSG-induced liver toxicity significantly. MSG at a dose of 4 mg/g significantly (P < 0.01) induced the formation of micronucleated polychromatic erythrocytes (MNPCEs). Co-treatment of rats with VIT C and quercetin inhibited the induction of MNPCEs by MSG (P < 0.001). VIT E failed to protect against MSG-induced genotoxicity. The results indicate that dietary antioxidants have protective potential against oxidative stress induced by MSG and, in addition, suggest that active oxygen species may play an important role in its genotoxicity.
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PMID:Monosodium glutamate-induced oxidative damage and genotoxicity in the rat: modulatory role of vitamin C, vitamin E and quercetin. 1802 56

The following parameters were determined in blood serum of apparently healthy Bennett's wallabies (Macropus rufogriseus) using the Hitachi 917 (Roche Diagnostics, Mannheim, Germany) and/or the Vettest 8008 (IDEXX-GmbH, Woerrstadt, Germany): alkaline phosphatase, alanine aminotransferase, ammonia, alpha-amylase, aspartate aminotransferase, Ca, Cl, cholesterol, cholinesterase, creatine kinase, creatinine, gammaglutamyltransferase, glucose, iron, lactate dehydrogenase, magnesium, phosphate, potassium, protein, sodium, total bilirubin, triglyceride, and urea. The results for cholesterol, glucose, total protein, triglyceride and for the enzymes alanine aminotransferase, alkaline phosphatase, aspartate aminotransferase, gamma-glutamyltransferase and lactate dehydrogenase differed significantly between both methods (P < 0.05). There is a negative correlation between the age of the Bennett's wallabies and the activity of the alkaline phosphatase. Five protein fractions could be separated on cellulose acetate electrophoresis. The mean concentrations of fructosamine and beta-hydroxybutyrate were 447.3 micromol/L and 0.27 mmol/L, respectively. The estimated vitamin A intake had no influence on the vitamin A concentration in serum. The serum vitamin E concentration was in general low and vitamin E was below the detection limit of 0.82 micromol/L in 29 out of 42 serum samples. The use of these analytes is discussed concerning the knowledge about the physiology, nutrition and diseases of macropods.
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PMID:On the clinical chemistry of the Bennett's wallaby (Macropus rufogriseus rufogriseus). 1685 6

The objective of this study was to evaluate the protective immunity of excretory-secretory products of Fasciola hepatica (FhES) worm against S.mansoni infection in mice. Evaluation of FhES antigen was through measuring worm burden, ova count, granuloma size and frequency as well as the histopathological picture of the liver. The study was extended to determine the level of free radical scavengers; lipid peroxide, glutathione (GSH), vitamin C, vitamin E, catalase and superoxide dismutase (SOD). Liver function enzymes such as aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP) were also taken into consideration. Four groups of eight mice each were selected for this study. Group 1 served as control group. Group 2: normal healthy mice vaccinated with FhES product. Group 3: S.mansoni infected mice for 2 months and group 4: infected mice pre-vaccinated with FhES antigen. Vaccination schedule comprised of a single subcutaneous injection of FhES antigen emulsified with Freund's complete adjuvant in a dose 0.5 mg protein/mouse, followed by intraperitoneal injections of the same antigen without adjuvant in 3 doses/week for 3 successive weeks. The total antigen inoculation was 5 mg protein/mouse. The present results revealed a drastic change in all the measured parameters after S.mansoni infection and a noticeable improved level after vaccination with FhES antigen. It can be concluded that FhES antigen succeeded to protect mice against schistosomiasis by a significant reduction in worm burden, ova count, granuloma size and number, improvement in the histopathological architecture of the liver as well as amelioration in the antioxidant levels under investigation.
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PMID:Excretory-secretory product of fasciola hepatica worm protects against Schistosoma mansoni infection in mice. 1687 44

It is well known that formaldehyde (FA) and reactive oxygen species (ROS) are cytotoxic and potentially carcinogenic. Although the individual effects of these reactants on cells have been investigated, the cytotoxicity exerted by the coexistence of FA and ROS is poorly understood. The present study was carried out to evaluate oxidant/antioxidant status and biochemical changes occurring after chronic formaldehyde toxicity in liver tissue and plasma of rats and protective effect of vitamin E (vit E) against oxidative damage. Eighteen rats were divided into three groups: (1) control rats, (2) rats treated with FA (FAt), and (3) rats treated with FA plus vit E (FAt + vit E) groups. After the treatment, the animals were sacrificed and liver tissues were removed for biochemical investigations. As a result, FA treatment significantly increased the levels of tissue malondialdehyde (MDA), protein carbonyl (PC), nitric oxide (NO) and the activity of xanthine oxidase enzyme (XO). On the other hand, FA exposure led to decrease in superoxide dismutase (SOD) and catalase (CAT) activities in liver tissues compared to control. FA caused significant decreases in total protein (TP) and albumin (ALB) whereas increases in aspartate transaminase (AST), alanine aminotransferase (AST), alkaline phosphatase (ALP) and interleukine-2 (IL-2) levels in plasma. Vit E treatment abolished these changes at a level similar to the control group. It was concluded that vit E treatment might be beneficial in preventing FA-induced liver tissue damage, and therefore have potential for clinical use.
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PMID:Vitamin E protects against oxidative damage caused by formaldehyde in the liver and plasma of rats. 1693 16

Monosodium glutamate (MSG), administered to rats (by gavage) at a dose of 0.6 mg/g body weight for 10 days, significantly (P<0.05) induced lipid peroxidation (LPO), decreased reduced glutathione (GSH) level and increased the activities of glutathione-s-transferase (GST), catalase and superoxide dismutase (SOD) in the liver of the animals; these were observed 24 hr after 10 days of administration. The activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and gamma glutamyl transferase (GGT) were also significantly increased in the serum, on MSG administration. Vitamin E (0.2 mg/g body wt) co-administered with MSG, significantly reduced the LPO, increased the GSH level and decreased the hepatic activities of GST, catalase and SOD. The activities of ALT, AST and GGT in the serum were also significantly reduced. The results showed that MSG at a dose of 0.6 mg/g body wt induced the oxidative stress and hepatotoxicity in rats and vitamin E ameliorated MSG-induced oxidative stress and hepatotoxicity.
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PMID:Effect of vitamin E on monosodium glutamate induced hepatotoxicity and oxidative stress in rats. 1695 47

Diabetes is associated with hyperglycemia, one of the most important causes of oxidative stress. Endogenous antioxidants are able to destroy the reactive species and create a balance between antioxidant and free radicals. In diabetes, the oxidative stress is increased due to the deficiency in the antioxidant defense. The intake of antioxidants, such as vitamin E, may reduce the oxidative stress associated with diabetes and hence help to restore the antioxidant defense system. The aim of this article was to investigate the effect of different doses of vitamin E on the biochemical parameters of normal and streptozotocin (STZ)-induced diabetic rats. Biochemical analysis was used to study the effect of this vitamin on the biochemical parameters of normal and diabetic rats. The plasma levels of alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactic dehydrogenase (LDH), and gamma-glutamyl transferase (gamma-GT) were significantly increased after the onset of diabetes. In addition, STZ-induced diabetes also caused an increase in the level of blood urea nitrogen (BUN) and creatinine. Oral administration of vitamin E (0.2-0.4 mg daily) significantly (P < 0.05) decreased the plasma level of ALT, AST, and gamma-GT. In addition, there was a slight but not significant reduction in the plasma level of ALP. Parameters of kidney function, such as BUN and creatinine, were slightly reduced after the oral administration of vitamin E. The plasma level of electrolytes, such as calcium and sodium, also changed significantly (P < 0.00001) after the oral administration of vitamin E. Vitamin E ameliorates the metabolic and biochemical parameters of diabetic rats.
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PMID:Vitamin E ameliorates some biochemical parameters in normal and diabetic rats. 1715 19

Steers and bulls under feedlot conditions and on an apparently adequate ration developed transitory signs of diarrhea and unthriftiness. One animal became recumbent. Sick and clinically normal animals in the group had elevated serum creatine kinase and aspartate aminotransferase enzyme values and degenerative changes in muscle fibers on biopsy. Feed analysis was carried out and the animals were monitored over several weeks by means of muscle biopsy and serum enzyme analysis as well as by postmortem examination at slaughter. Subclinical myopathy was found in several animals and was thought to be related to low vitamin E content in the high moisture corn ration.
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PMID:A nutritional myopathy enzootic in a group of yearling beef cattle. 1742

We examined how oxidative stress and cell damage develop in the liver of rats subjected to water-immersion stress (WIRS). In rats subjected to WIRS for 1.5, 3 or 6 h, serum alanine aminotransferase and aspartate aminotransferase activities increased time-dependently. In the liver tissue, vacuolization and apoptosis occurred at 1.5 h of WIRS and vacuolization further developed without further appearance of apoptosis at 3 h or 6 h. Serum lipid peroxide (LPO) and NOx (nitrite/nitrate) concentrations increased at 3 h of WIRS and these increases were enhanced at 6 h. In liver tissue, increases in LPO and NOx concentrations and myeloperoxidase activity and decreases in ascorbic acid and reduced glutathione concentrations and superoxide dismutase activity occurred at 3 h of WIRS and these changes were enhanced at 6 h, although vitamin E concentration and xanthine oxidase activity were unchanged. These results indicate that oxidative stress in the liver of rats with WIRS develops after the appearance of cell damage in the tissue, and suggests that oxidative stress is caused through disruption of the antioxidant defense system and increases in NO generation and neutrophil infiltration in the liver, which may contribute to the progression of cell damage in the tissue.
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PMID:Development of oxidative stress and cell damage in the liver of rats with water-immersion restraint stress. 1762 21


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