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)

Ischemia and reperfusion injury of the skeletal muscle is a common and serious condition observed in patients admitting to peripheral vascular surgery, interventional radiology and cardiology departments. Resveratrol (RVT) being a strong natural antioxidant is found in deal of red wine and Mediterranean diet. In the present study, male Spraque-Dawley rats were randomized into two groups of equal size. The first group was the control group, and these rats were administered with tap water with a gastric tube for fourteen consecutive days once daily. According to the same protocol, the rats in the second group were treated with tap water containing 20 mg/kg RVT. All the rats in the two groups were subjected to acute hind limb ischemia through clamping of the abdominal aorta for 120 min. Following this procedure, 60 minutes of reperfusion was applied by reestablishing blood flow in both iliac arteries. Ischemic damage in the skeletal muscle tissue was assessed by measuring myoglobin, lactate dehydrogenase, creatinine phosphokinase, aspartate transaminase enzymes in venous blood samples obtained at the end of the reperfusion period. Oxidative stress caused by reperfusion was determined by measuring MDA, carbonyl and protein sulphydryl levels in quadriceps muscle tissue retrieved at the end of the experiment. In Group II rats, all the measured ischemic enzymes and the markers of oxidative stress reflected robust anti-ischemic properties obtained by RVT administration. The data from both groups revealed statistically significant protection against acute skeletal muscle ischemia and reperfusion injury in Group II rats, compared to Group I. As a major dietary flavonoid RVT can protect the skeletal muscle tissue against global ischemia and reperfusion injury because of its strong antioxidant and cytoprotective properties.
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PMID:Protective effects of resveratrol in ischemia-reperfusion injury of skeletal muscle: A clinically relevant animal model for lower extremity ischemia. 1705 53

Cisplatin (CDDP) is a widely used anticancer drug, but at high dose, it can produce undesirable side effects such as hepatotoxicity. Because silymrin has been used to treat liver disorders, the protective effect of silymarin on CDDP-induced hepatotoxicity was evaluated in rats. Hepatotoxicity was determined by changes in serum alanine aminotransferase [ALT] and aspartate aminotransferase [AST], nitric oxide [NO] levels, albumin and calcium levels, and superoxide dismutase [SOD], glutathione peroxidase [GSHPx] activities, glutathione content, malondialdehyde [MDA] and nitric oxide [NO] levels in liver tissue of rats. Male albino rats were divided into four groups, 10 rats in each. In the control group, rats were injected i.p. with 0.2 ml of propylene glycol in saline 75/25 (v/v) for 5 consecutive days [Silymarin was dissolved in 0.2 ml of propylene glycol in saline 75/25 v/v]. The second group were injected with CDDP (7.5 mg /kg, I.P.), whereas animals in the third group were i.p. injected with silymarin at a dose of 100 mg/kg/day for 5 consecutive days. The Fourth group received a daily i.p. injection of silymarin (100 mg/kg/day for 5 days) 1 hr before a single i.p. injection of CDDP (7.5 mg/kg). CDDP hepatotoxicity was manifested biochemically by an increase in serum ALT and AST, elevation of MDA and NO in liver tissues as well as a decrease in GSH and the activities of antioxidant enzymes, including SOD, GSHPx in liver tissues. In addition, marked decrease in serum NO, albumin and calcium levels were observed. Serum ALT, AST, liver NO level, MDA was found to decreased in the combination group in comparison with the CDDP group. The activities of SOD, GSHPx, GSH and serum NO were lower in CDDP group than both the control and CDDP pretreated with silymarin groups. The results obtained suggested that silymarin significantly attenuated the hepatotoxicity as an indirect target of CDDP in an animal model of CDDP-induced nephrotoxicity.
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PMID:Silymarin modulates Cisplatin-induced oxidative stress and hepatotoxicity in rats. 1712 99

The hepatoprotective effect of ethanolic extract and its four different fractions (CHCl(3), EtOAc, n-BuOH, and remaining water fraction) of Vitis vinifera L. leaves was investigated against carbon tetrachloride (CCl(4))-induced acute hepatotoxicity in rats. The ethanolic extract was found active at 125mg/kg dose (per os). The ethanolic extract was fractionated through successive solvent-solvent extractions and the n-BuOH fraction in 83mg/kg dose possessed remarkable antioxidant and hepatoprotective activities. Liver damage was assessed by using biochemical parameters (plasma and liver tissue MDA [malondialdehyde], transaminase enzyme levels in plasma [AST-aspartate transaminase, ALT-alanine transferase] and liver GSH [glutathione] levels). Additionally, the pathological changes in liver were evaluated by histopathological studies. Legalon 70 Protect was used as standard natural originated drug.
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PMID:Hepatoprotective effect of Vitis vinifera L. leaves on carbon tetrachloride-induced acute liver damage in rats. 1739 82

This study was designed to investigate the protective effects of two traditionally used Turkish medicinal plants, Camellia sinensis (CS) and Urtica dioica L. (UD), beverages used against chemical carcinogen trichloroacetic acid (TCA)-exposure in rats. The preventive potential of the plant infusions was evaluated by measuring the level of serum marker enzymes, aspartate aminotransferase (AST), alanine aminotransferase (ALT), creatine phosphokinase (CPK), acid phosphatase (ACP), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH); antioxidant defense systems, reduced glutathione (GSH), glutathione reductase (GR), superoxide dismutase (SOD), glutathione-S-transferase (GST) and catalase (CAT); and lipid peroxidation (malondialdehyde, MDA) content in various organs of rats. Twenty four healthy rats were randomly allotted into four experimental groups: A (untreated control), B (only TCA-treated), C (TCA+CS treated) and D (TCA+UD treated). At the end of the 50 days, the plant infusions possessed chemoprotective effects, deduced by the remaining TCA-induced increased serum damage marker enzyme, lipid peroxidation and antioxidative system in rats compared with those of the control and TCA-exposed rats. According to the results, while the levels of AST, ALT and CPK increased in group B, no significant changes were observed in groups C and D. The MDA content slightly increased in tissues of all groups, being higher in group B. Antioxidant enzyme activities such as SOD and CAT increased significantly in the brain, liver and kidney of group B while they did not change significantly except for in the kidney in groups C and D. The GSH level and the ancillary enzyme GR activity did not change significantly in organs of all groups. On the other hand, the drug metabolizing enzyme, GST, activity decreased significantly in the brain, liver and kidney of group D while slight changes were observed for the other groups. The results revealed that TCA exposure induced oxidative stress in rat tissues, however, in plant beverage supplemented groups, a significant protective effect of CS and UD against TCA-induced oxidative injury was recorded. Hence, the study revealed that the constituents present in CS and UD impart protection against carcinogenic chemical induced oxidative injury that may result in the development of cancer. Also the observations, along with changes, suggest that both CS and UD may possess preventive potential during a 50-day protective exposure.
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PMID:Elevation protective role of Camellia sinensis and Urtica dioica infusion against trichloroacetic acid-exposed in rats. 1762 76

Today's world is increasingly seeking ways to replace the synthetic drugs with the therapeutic power of natural products. This study was designed to investigate the protective effects of Foeniculum vulgare (FV) and Salvia officinalis (SO) waters infusions against carcinogen chemical trichloroacetic acid (TCA)-exposure in rats. The chemopreventive potential of the plant infusions were evaluated by measuring levels of serum marker enzymes [aspartate aminotransferase (AST), alanin aminotransferase (ALT), creatine phosphokinase (CPK), acid phosphatase (ACP), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH)], antioxidant defense systems [Reduced glutathione (GSH), glutathione reductase (GR), superoxide dismutase (SOD), glutathione-S-transferase (GST) and catalase (CAT)] and lipid peroxidation level (Malondialdehyde = MDA) in various tissues of rats. Female Sprague-Dawley rats, weighing 150-200 g, were randomly allotted into four experimental groups. While the control group (A) received only natural spring water, the treatment B group (0.2% TCA) supplied with the drinking water containing 0.2% TCA, the treatment C (TCA + FV infusion) and D (TCA + SO infusion) groups drank the drinking water containing 0.2% TCA and 2.5% the plant grains and leaves ad libitum for 50 days during experiment. At the end of the 50 days experiment, TCA and the plant's infusions caused different affect on the serum marker enzymes, tissues antioxidant defense systems and lipid peroxidation against TCA-exposed in rats with comparison to those of TCA exposed and control rats. According to the results, both TCA and TCA + plants infusions caused a significant increase in serum AST, ALT and CPK activity. Non-enzymic antioxidant GSH level significantly increased in the brain whereas reduced in the erythrocytes and kidney of TCA + FV and TCA + SO as compared to TCA group and control. While MDA content slightly increased in tissues of TCA group in comparison to those of control, significantly decreased in the brain, liver and kidney of rats of TCA + FV and TCA + SO groups as compared to TCA group and control. Antioxidative enzyme activity such as CAT and SOD significantly increased in the brain, liver and kidney tissues of TCA induced group whereas reduced the same enzymes activities as compared to TCA group. The ancillary enzyme GR activity significantly depleted in the brain and kidney of TCA + FV and TCA + SO groups in comparison to those of TCA exposed and control rats. In addition, the drug metabolizing enzyme GST activity significantly declined in the brain and kidney of TCA + FV and TCA + SO groups in comparison to those of TCA exposed and control rats, whereas, also reduced in the liver of TCA + FV and TCA + SO groups in comparison to those of TCA exposed rats. It was concluded that the levels of serum marker enzymes were found not to be decreased in plants treated groups due to hepatic damage induced by TCA. Also the four antioxidant enzymes were found to be activated in different degrees following TCA treatment and declined the activation of the enzymes the plant infusions accompanied by significant reduction in MDA concentration in the tissues. The observations, along with changes, might suggest that the both FV and SO may possess antioxidant properties during the period of a 50-day protective exposure.
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PMID:Determination of chemopreventive role of Foeniculum vulgare and Salvia officinalis infusion on trichloroacetic acid-induced increased serum marker enzymes lipid peroxidation and antioxidative defense systems in rats. 1799 40

1. An experiment was conducted to study the effect of thiram on liver antioxidant capacity and incidence of tibial dyschondroplasia in broilers. 2. One hundred and twenty Avian commercial broilers were allotted at random to three treatments: control group, low thiram group (50 mg/kg) and high thiram group (100 mg/kg). 3. Blood samples were collected to determine the activity of AST (aspartate aminotransferase). At the end of the trial, broilers were killed and liver samples were collected to determine the activity of SOD (superoxide dismutase), GSH-Px (glutathione peroxidase) and MDA (malondialdehyde) content, while the right proximal tibiotarsi were dissected in longitudinal section for assessment of tibial dyschondroplasia (TD) incidence and TD score. 4. The results showed that thiram increased the incidence of TD and TD scores, increased serum AST activity and MDA content of liver, and decreased the activity of SOD and GSH-Px in the liver. 5. They suggest that thiram causes TD in broilers by reducing liver antioxidation capability and damaging liver function; this may be one of the mechanisms by which thiram causes TD in broilers.
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PMID:Effect of diet with thiram on liver antioxidant capacity and tibial dyschondroplasia in broilers. 1808 55

Although IPC (ischaemic preconditioning) is considered as a protective strategy in HI/R (hepatic ischaemia/reperfusion), the mechanisms for this effect have not been fully elucidated. In the present study we investigate whether PPC (pharmacological preconditioning) by transient activation of A(1)R (adenosine A(1) receptor) protects against long-term HI/R and whether the protective effects of IPC depend on A(1)R activation and whether both preconditionings affect remote organs. Wistar rats underwent IPC and long-term HI/R. Another set of animals were pharmacologically preconditioned with the A(1)R-agonist CCPA [2-chloro-N(6)-cyclopentyladenosine; 0.1 mg/kg of body weight, i.p. (intraperitoneally)] 24 h before HI/R. In other groups, rats received an A(1)R-antagonist, DPCPX (1,3-dipropyl-8-cyclopentylxanthine; 0.1 mg/kg of body weight, i.p.) 24 h before HI/R. Hepatic damage was evaluated by transaminase [AST (aspartate transaminase), ALT (alanine transaminase)] release; inflammation was assessed by hepatic MPO (myeloperoxidase) and serum TNFalpha (tumour necrosis factor alpha) and NO; oxidative stress was estimated by MDA (malondialdehyde) and 4-HDA (4-hydroxyalkenals), SOD (superoxide dismutase) activity, GSH and ADA (adenosine deaminase) as adenosine metabolism. Both preconditionings protected liver and lung against HI/R as indicated by the reduction in transaminases, MPO, MDA+4-HDA, NO, TNFalpha and ADA activity as compared with HI/R (P<0.05). However, pre-treatment with DPCPX abolished the protective effects of IPC and PPC. Preconditionings induced a significant increase in hepatic MnSOD (manganese SOD) activity and NO generation compared with the sham group, and this activity was abolished by DPCPX pre-treatment. A(1)R activation induced hepatic delayed preconditioning and blockade of A(1)R abolished hepatic IPC. IPC, as well as PPC, were able to prevent lung damage. These protective effects are associated with a reduction in oxidative stress, inflammation and endogenous antioxidant preservation.
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PMID:Ischaemic and pharmacological preconditionings protect liver via adenosine and redox status following hepatic ischaemia/reperfusion in rats. 1830 14

Pringle described a new technique to reduce blood loss during liver surgery. Adult Wistar rats were subjected to 1 h of partial liver ischemia and followed by 3 h reperfusion. Eighteen Wistar rats were divided into sham-operated control group (I) (n=6), ischemia and reperfusion (I/R) group (II) (n=6), L-arginine treated group (100 mg/kg body weight/daily by oral route for 7 d before induced ischemia reperfusion maneuver) (III) (n=6). Ischemic and reperfusion hepatocellular injury occurred as indicated by increased-alanine transaminase (ALT), aspartate transaminase (AST). Pre-treatment with L-arginine significantly decreased serum-ALT, AST after 1 h ischemia followed by 3 h of reperfusion. Nitric oxide production, in hepatocytes was increased 2 fold and MDA levels significantly decreased by L-arginine treatment as compared to I/R rat. Histopathology and TEM studies showed markedly diminished hepatocellular injury in L-arginine pretreated rats during the hepatic I/R, which reached a level comparable to saline-treated rat of sham operated group. Thus, findings it may be concluded that L-arginine afforded significant protection from hepatobiliary function from I/R injury by nitric oxide production.
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PMID:L-arginine protects from pringle manoeuvere of ischemia-reperfusion induced liver injury. 1845 13

Cyclosporine A (CyA) leads to liver injury, probably by causing the production of free radicals and resulting in nitric oxide (NO) deficiency. We evaluated CyA-mediated liver damage histopathologically to determine the possible beneficial effects of L-arginine (L-Arg). In this study, 7 groups of Sprague-Dawley rats; (1) Control group; (2) 0.9% NaCl group; (3) CyA group: 7.5mg/kg/day; (4) L-Arg group: 2g/lt/day; (5) l-NAME (N-nitro-L-arginine methyl ester) group: 5mg/100ml/day; (6) CyA+L-Arg group: L-Arg (2g/lt/day)+CyA (7.5mg/kg/day); and (7) CyA+L-NAME group: CyA (7.5mg/kg/day)+L-NAME (5mg/100ml/day) were included. At the end of the treatments, animals were killed and hepatic tissues were treated for morphological (hematoxylin and eosin) and biochemical (NO and malondialdehyde, MDA) analyses, and serum was processed for biochemical (alanine transaminase (ALT), aspartate transaminase (AST), bilirubin, alkaline phosphatase (ALP) and total protein) study. The results indicated that CyA-induced hepatotoxicity was characterized by sinusoidal dilatation, hepatocellular vacuolization, neutrophilic infiltration and hepatocellular necrosis. These findings were less pronounced in the CyA+L-Arg group than CyA alone group. L-NAME group showed moderate changes. The CyA+L-NAME (Group 7) had more severe changes. We found changes in tissue NO and MDA levels. We think that the tissue damage caused by CyA is mild and reversible at the period when biochemical parameters are just starting to become abnormal and that L-Arg may have a protective effect against CyA damage on liver.
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PMID:Oral L-arginine protects against cyclosporine-induced hepatotoxicity in rats. 1858 16

Cisplatin-induced oxidative stress can cause liver and kidney damage, thus limiting therapeutic efficacy. Thus, in the present study, since Rhus verniciflua Stokes (RVS) containing flavonoids has antioxidant effects, we investigated whether it can protect cisplatin-induced toxicity in vitro and in vivo, The in vitro effects of RVS on the cell viability and reactive oxygen species (ROS) production were investigated using cisplatin-treated Madin-Darby Canine kidney (MDCK)-I renal cells. Its in vivo effects were also studied in BALB/c mice inoculated with CT-26 colon adenocarcinoma cells and treated with cisplatin with or without RVS. Liver and renal functions were assessed together with indices of tissue oxidation. RVS prevented cisplatin-induced cytotoxicity and ROS release against MDCK-I cells. RVS alone exerted modest antitumor activity against CT-26 cells. When used concurrently with cisplatin, RVS prevented the increases in serum blood urea nitrogen (BUN), creatinine, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and NO, while reducing liver and kidney tissue MDA content, and increasing catalase, glutathione (GSH), and superoxide dismutase (SOD) activities. Moreover, the antitumor efficacy of cisplatin was not altered by concurrent administration of RVS. These findings demonstrate that RVS prevents cisplatin-induced toxicity in vitro and in vivo via an antioxidant activity without hurting its antitumor effectiveness, suggesting that RVS can be usefully applied to the neoplastic patients as a combined chemopreventive agent with cisplatin.
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PMID:Rhus verniciflua Stokes prevents cisplatin-induced cytotoxicity and reactive oxygen species production in MDCK-I renal cells and intact mice. 1915 Feb 36


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