Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Caffeic acid is a well-known phenolic compound mainly present in plants. In this study, caffeic acid was evaluated for its protective effect against chronic ethanol-induced biochemical changes in male Wistar rats. Administration of ethanol (7.9 g/kg/day) for 45 days induced liver and kidney damage as manifested by a significant increase in the levels of serum hepatic and renal markers namely aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), gamma glutamyl transferase (GGT), bilirubin, urea, creatinine, and a significant decrease in creatinine clearance and levels of hemoglobin. Plasma thiobarbituric acid-reactive substances and hydroperoxide were significantly elevated where as the levels of nonenzymic antioxidants [reduced glutathione, vitamin E and vitamin C] were significantly decreased in alcohol-intoxicated rats. Administration of caffeic acid along with alcohol significantly decreased the serum levels of liver and kidney markers to near-normal levels. In addition, administration of caffeic acid significantly decreased the levels of lipid peroxidation markers while the levels of antioxidants were significantly increased in circulation of alcohol-fed rats. All these results were accompanied by histological observations in liver. The results demonstrate that caffeic acid has a beneficial effect in reducing the adverse effect of alcohol.
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PMID:Protective role of caffeic acid against alcohol-induced biochemical changes in rats. 1763 73

The protective efficacy of diallyl tetrasulfide (DTS) from garlic on liver injury induced by cadmium (Cd) was investigated. In this study, Cd (3 mg/kg body weight) was administered subcutaneously for 3 weeks to induce toxicity. DTS was administered orally (10, 20 and 40 mg/kg body weight) for 3 weeks with subcutaneous (sc) injection of Cd. Cd-induced liver damage was evidenced from increased activities of serum hepatic enzymes, namely aspartate transaminase, alanine transaminase, alkaline phosphatase and lactate dehydrogenase, with significant elevation of lipid peroxidation indices (thiobarbituric acid reactive substances and hydroperoxides) and protein carbonyl groups in the liver. Rats subjected to Cd toxicity also showed a decline in the levels of total thiols, reduced glutathione (GSH), vitamin C and vitamin E, accompanied by an increased accumulation of Cd, and significantly decreased activities of superoxide dismutase, catalase (CAT), glutathione peroxidase, glutathione-S-transferase (GST), glutathione reductase, and glucose-6-phosphate dehydrogenase in the liver. Administration of DTS at 40 mg/kg body weight significantly normalised the activities of hepatic marker enzymes, compared to other doses of DTS (10 and 20 mg/kg body weight). In addition, DTS (40 mg/kg body weight) significantly reduced the accumulation of Cd and the level of lipid peroxidation, and restored the level of antioxidant defense in the liver. Histological studies also showed that administration of DTS to Cd-treated rats resulted in a marked improvement of hepatocytes morphology with mild portal inflammation. Our results suggest that DTS might play a vital role in protecting Cd-induced oxidative damage in the liver.
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PMID:Effects of diallyl tetrasulfide on cadmium-induced oxidative damage in the liver of rats. 1769 48

An in vitro study using rabbit sperm was designed to evaluate the cytotoxic effects of different concentrations of aluminium chloride (AlCl(3)) at 0, 2 and 4h of incubation on sperm motility and viability, oxidative status and the activities of some antioxidant enzymes (superoxide dismutase (SOD) and catalase (CAT)), transaminases and acid phosphatase. The role of vitamin C (1 mM) or vitamin E (2 mM) was also investigated in counteracting deterioration caused by AlCl(3) on the tested parameters. Rabbit sperm was incubated with different concentrations of AlCl(3) (0, 1, 5, 10, 15 and 20 mM) with or without vitamin C or vitamin E for 2 and 4 h. Results revealed that the percentage of motile and viable sperm decreased significantly after AlCl(3) treatment at 10, 15 and 20 mM and the response was both concentration and time dependent. Aluminium chloride at concentrations of 10, 15 and 20 mM caused significant induction of oxidative stress as evidenced by increased thiobarbituric acid reactive substances (TBARS) levels and inhibition in the activities of SOD and CAT. Increase in the activities of aspartate transaminase (AST) and alanine transaminase (ALT) and decline in the activity of acid phosphatase (ACP) were also observed at AlCl(3) concentrations of 15 and 20 mM. Co-incubation with either vitamin C or vitamin E resulted in marked degrees of protection against AlCl(3)-induced cytotoxic effects, represented in decreased TBARS levels and restoration of enzymes activities near control. On the other hand, no significant effect was exerted from vitamin C or vitamin E on motility and viability. The present study demonstrated that AlCl(3) caused deterioration in sperm motility and viability, enhancement of free radicals and alterations in enzymes activities. The antioxidants revealed protective effects against the cytotoxicity of AlCl(3).
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PMID:An in vitro study on reproductive toxicity of aluminium chloride on rabbit sperm: the protective role of some antioxidants. 1771 45


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