UNIPROT:P17174 - FACTA Search

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)

Halothane is an important human and veterinary anesthetic, which produces free radicals during biotransformation. Occasionally, these free radicals may cause hepatic injury, especially in case of multiple halothane exposures over short periods. Vitamin C may protect cellular lipids and lipoproteins against oxidative damage by the free radicals. This study investigated the effects of vitamin C on liver enzymes and other biochemical parameters in rats anesthetized with halothane. One group of rats was used as a control, and saline (0.9% NaCl) was injected intraperitoneally into these animals as a placebo. The second group of rats was used as an anesthesia control group and was only anesthetized by halothane for 2 h. The third group was anesthetized by halothane and injected vitamin C intraperitoneally. Activities of aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase enzymes were significantly increased (p < 0.05, p < 0.01, p < 0.05, respectively) by halothane anesthesia, but decreased (p < 0.05, p < 0.05, p < 0.05, respectively) with administration of vitamin C. Concentrations of triglycerides, cholesterol, total bilirubin and creatinine were statistically affected (p < 0.05, p < 0.01, p < 0.05, and p < 0.01, respectively) by injection of vitamin C. Values of erythrocyte counts, packet cell volumes, hemoglobin concentration, leukocyte counts, rates of neutrophils and lymphocytes were significantly affected (p < 0.01, p < 0.05, p < 0.05, p < 0.01, p < 0.001 and p < 0.01, respectively) by halothane anesthesia. The values of erythrocyte counts, leukocyte counts, neutrophil and lymphocyte rates were significantly decreased (p < 0.05, p < 0.05, p < 0.05, p < 0.01 and p < 0.01, respectively) with administration of vitamin C. Based upon these results, vitamin C may play an important role in the prevention of hepatic cellular injury inflicted by halothane anesthesia.
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PMID:Effects of vitamin C on liver enzymes and biochemical parameters in rats anesthetized with halothane. 1590 86

We have evaluated the comparative effect of curcumin (diferuloyl methane) and its analogue [bis-1,7-(2-hydroxyphenyl)-hepta-1,6-diene-3,5-dione] (BDMC-A) on carbon tetrachloride-induced hepatotoxicity in rats. Administration of carbon tetrachloride (3 ml/kg/week) for three months significantly (P<0.05) increased the levels of marker enzymes such as aspartate transaminase (AST), alkaline phosphatase (ALP) and gamma-glutamyl transferase (GGT). The levels of plasma thiobarbituric acid reactive substances (TBARS) and lipid hydroperoxides were also significantly (P<0.05) increased. We have observed a significant (P<0.05) decrease in the levels of plasma reduced glutathione (GSH), vitamin C and vitamin E. There was a significant (P<0.05) increase in the levels of TBARS and hydroperoxides in liver and kidney and a significant (P<0.05) decrease in the activities of enzymic antioxidants- superoxide dismutase (SOD), catalase and GSH peroxidase along with GSH in CCl(4)-treated rats. Oral administration of curcumin and BDMC-A to CCl(4)-induced rats for a period of three months significantly (P<0.05) decreased the levels of marker enzymes, plasma TBARS and hydroperoxides and increased the levels of plasma and tissue antioxidants. Histopathological studies of liver also showed protective effect of curcumin and BDMC-A. We have observed thickening of blood vessels and microvesicular fatty changes around the portal triad in CCl(4)-treated rat liver. Treatment with curcumin showed only mild sinusoidal dilatation while with BDMC-A there was only mild portal inflammation. The effect exerted by BDMC-A was found to be more promising than curcumin.
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PMID:Comparative effects of curcumin and an analogue of curcumin in carbon tetrachloride-induced hepatotoxicity in rats. 1594 54

Methanol is primarily metabolized by oxidation to formaldehyde and then to formate. These processes are accompanied by formation of superoxide anion and hydrogen peroxide. This paper reports data on the effect of methanol on antioxidant status and lipid peroxidation in lymphoid organs such as the spleen, thymus, lymph nodes and bone marrow of rats. Male Wistar albino rats were intoxicated with methanol (2.37 g/kg b.w intraperitoneally) for detecting toxicity levels for one day, 15 d and 30 d, respectively. Administration of methanol at 15 and 30 d significantly (p<0.05) increased lipid peroxidation and decreased the enzymatic (superoxide dismutase, catalase, glutathione peroxidase) and non-enzymatic antioxidants (reduced glutathione and vitamin C) in lymphoid organs. However, lipid peroxidation and enzymatic and non-enzymatic antioxidants in the acute methanol exposed group animals were found to be significantly (p<0.05) increased. In one day methanol intoxication, the levels of free radicals initially increased, and to remove these free radicals, antioxidants levels were elevated, which generally prevented oxidative cell damage. But in longer periods of intoxication, when the generation of reactive free radicals overwhelmed the antioxidant defense, lipid peroxidation increased. Further, decreased antioxidants in 15 and 30 d methanol intoxication may have been due to overutilization of non-enzymatic and enzymatic antioxidants to scavenge the products of lipid peroxidation. In addition, the liver and kidney markers of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), urea and creatinine significantly increased. This study concludes that exposure to methanol causes oxidative stress by altering the oxidant/antioxidant balance in lymphoid organs of the rat.
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PMID:Methanol-induced oxidative stress in rat lymphoid organs. 1648 59

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

The consumption of diets rich in plant foods is associated with a reduced risk of cardiovascular diseases. This study aimed to evaluate the preventive role of rutin on lipid peroxides and antioxidants in normal and isoproterenol-induced myocardial infarction in rats. Subcutaneous injection of isoproterenol (150 mg kg(-1)) to male Wistar rats at an interval of 24 h for two days showed a significant increase in the activity of serum cardiac marker enzymes (creatine kinase, lactate dehydrogenase, aspartate transaminase and alanine transaminase) and a significant decrease in the activity of these enzymes in the heart. Lipid peroxidative products (thiobarbituricacid reactive substances and lipid hydroperoxides) were significantly increased and enzymic (superoxide dismutase, catalase and glutathione peroxidase) and non-enzymic (reduced glutathione and vitamin C) antioxidants showed a significant decrease in isoproterenol-treated rats. Pretreatment with rutin (40 or 80 mg kg(-1)) to isoproterenol-treated rats orally for a period of 42 days daily caused a significant effect. Administration of rutin to normal rats did not have any significant effect on any of the parameters studied. The results of our study show that rutin possesses antioxidant activity in isoproterenol-induced experimental myocardial infarction.
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PMID:Preventive effect of rutin, a bioflavonoid, on lipid peroxides and antioxidants in isoproterenol-induced myocardial infarction in rats. 1664 Aug 40

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 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

Carbon tetrachloride (CCl(4): 4 ml/kg body weight as a 1:1 mixture of CCl(4) and mineral oil) was orally administered to rats. After 12 h the activity of plasma AST (aspartate aminotransferase) and ALT (alanine aminotransferase) was significantly higher than that of the control group and plasma AST and ALT activities increased thereafter. These results indicated that the necrotic process was active at about 12 h and developed thereafter. After 2-24 h of CCl(4) administration, the hepatic level of vitamin C, the most sensitive indicator of oxidative stress, decreased significantly, indicating that oxidative stress was significantly enhanced as early as 2 h after CCl(4) intoxication and thereafter. Phosphorylated JNK (c-Jun NH(2)-terminal kinase) and phospho-ERK1/2 (extracellular signal-regulated kinase1/2) were significantly increased transiently 1-3 h after treatment with CCl(4), while phosphorylated p38 decreased significantly 1-24 h after CCl(4) treatment. These results indicated that the change in MAPKs (mitogen activated protein kinases) slightly preceded that in vitamin C, the most sensitive chemical indicator of oxidative stress.
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PMID:Activation of mitogen activated protein kinase (MAPK) during carbon tetrachloride intoxication in the rat liver. 1728 12

Alcoholic liver disease (ALD) is one of the most common diseases in society. A large number of studies are in progress to identify natural substances that are effective in reducing the severity of ALD. 2-Hydroxy-4-methoxy benzoic acid (HMBA), the active principle of Hemidesmus indicus, an indigenous Ayurvedic medicinal plant in India, is expected to significantly inhibit the development of liver injury in ethanol administration. It is expected to reduce the severity of liver damage in terms of body weight, hepatic marker enzymes, oxidative stress, antioxidant status and histological changes in ethanol-induced hepatotoxic rats. Hepatotoxicity was induced by administering 20% ethanol (5 g kg(-1) daily) for 60 days to male Wistar rats, which resulted in significantly decreased body weight and an increase in liver-body weight ratio. The liver marker enzymes aspartate transaminase, alanine transaminase, alkaline phosphatase, gamma-glutamyl transpeptidase and lactate dehydrogenase were elevated. In addition, the levels of plasma, erythrocyte and hepatic thiobarbituric acid reactive substances, hydroperoxides and conjugated dienes were also elevated in ethanol-fed rats as compared with those of the experimental control rats. Decreased activity of superoxide dismutase, catalase, glutathione peroxidase, reduced glutathione, vitamin C and alpha-tocopherol was also observed on alcohol administration as compared with experimental control rats. HMBA was co-administered at a dose of 200 mug kg(-1) daily for the last 30 days of the experiment to rats with alcohol-induced liver injury, which significantly increased body weight, significantly decreased the liver-body weight ratio, transaminases, alkaline phosphatase, gamma-glutamyl transpeptidase and lactate dehydrogenase, significantly decreased the levels of lipid peroxidative markers, significantly elevated the activity of enzymic and non-enzymic antioxidants in plasma, erythrocytes and liver and also increased levels of plasma and liver vitamin C and alpha-tocopherol at the end of the experimental period as compared with untreated ethanol-administered rats. The histological changes were also in correlation with the biochemical findings. The results suggest that HMBA administration may afford protection against ethanol-induced liver injury in rats.
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PMID:Antioxidant effect of 2-hydroxy-4-methoxy benzoic acid on ethanol-induced hepatotoxicity in rats. 1733 49

Chlorpyrifos (CPF) is one of the most widely used organophosphorous insecticides in agriculture with its attendant adverse health outcomes. This study aimed at evaluating the effect of subchronic oral CPF administration on hematological and serum biochemical indices, and the possible ameliorating effect of vitamin C on the indices in mice. Thirty mice divided into 3 groups of 10 mice each were used for this study. Mice in group I (control) were dosed with vegetable oil, while those in group II were given CPF (21.3 mg/kg~ 1/5(th) LD(50)) only. Mice in group III were pretreated with vitamin C (100 mg/kg) prior to dosing with CPF 30 min later (Vitamin C + CPF-treated group). This regime was given to each group of mice three times a week for a period of ten weeks. During the study period, mice were examined for signs of toxicity, and weight of each mouse was measured every week. At the end of the study period, blood samples were collected from the mice and analyzed for packed cell volume (PCV), total red blood cell (RBC), white blood cell (WBC) and total protein (TP). Serum obtained from the blood was analyzed for Na( +, K+ and Cl-), urea, creatinine, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP). The results showed that mice in the vitamin C + CPF-treated group exhibited milder signs of toxicity and significant increase in weight gain (p<0.01) compared to the CPF-treated group. No significant increase in weight in the CPF-treated group was observed compared to the control. There was a significant increase in PCV, RBC, Hb, TP and creatinine, but a significant decrease was obtained in WBC, ALT and AST in the CPF-treated group compared to the control. All the parameters with the exception of WBC, ALT and AST (which increased significantly), were significantly decreased in the vitamin C + CPF-treated group compared to CPF-treated group. ALP was significantly elevated in the CPF-treated group compared to both the control and vitamin C + CPF-treated group. No significant changes in urea and the measured electrolytes in all three groups, except a significant decrease in the concentration of Na(+) was observed in the CPF-treated group compared to the control. The study demonstrated that pretreatment of CPF-administered mice with vitamin C significantly altered some important hematological and serum biochemical parameters, revealing the protective action of the vitamin against some organ damage induced by CPF.
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PMID:Evaluation of subchronic chlorpyrifos poisoning on hematological and serum biochemical changes in mice and protective effect of vitamin C. 1753 35

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