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)

L-carnitine is a cofactor in the transfer of long-chain fatty acid allowing the beta-oxidation of fatty acid in the mitochondria. It is also a known antioxidant with protective effects against lipid peroxidation. In this study, hepatoprotective effect of L-carnitine was investigated against acetaminophen (AA)-induced liver toxicity where mitochondrial dysfunction and oxidative stress are thought to be involved in AA hepatotoxicity. Sixty-four Balb/C mice were divided into eight groups. Mice were dosed with single-AA injection (500 mg/kg via the intra peritoneal route) with or without L-carnitine (500 mg/kg for 5 days starting 5 days before AA injection via intra peritoneal route) and sampled at 4, 8 and 24 h following AA injection. AA increased serum AST, ALT, total sialic acid (TSA) and MDA as well as tissue TSA and MDA levels significantly with the highest increase observed at 4 h, but there was a decrease in blood and tissue GSH level. Administration of L-carnitine significantly reduced AA-induced elevations in AST, ALT, TSA and MDA concentrations and increased GSH levels at all sampling points. AA also induced necrosis, hyperemia, sinusoidal congestion and hemorrhage with time-dependent increase in severity, but the degree of necrosis and histopathologic alterations were most severe at 24 h following AA administration. However, the degree of pathologic alterations was less severe with simultaneous L-carnitine application. These results suggest that AA results in oxidative damage in the liver with an acute effect. L-carnitine also has a prominent protective effect against AA toxicity and may be of therapeutic value in the treatment of AA-induced hepatotoxicity.
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PMID:Hepatoprotective effect of L-carnitine against acute acetaminophen toxicity in mice. 1771 80

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

To assess the effects of anti-TNF-alpha antibody (infliximab) in experimental steatohepatitis induced by methionine- and choline-deficient (MCD) diet. The study included thirty rats. One group received normal rat food, and two groups received MCD diet. The treatment group received a single dose intra-peritoneal infliximab (4 mg/kg), at week 8. MCD diet increased levels of AST, ALT, TNF-alpha, TGF-beta(1), tissue and plasma MDA (p < 0.05 for each). Moreover, it led to steatosis, ballooning degeneration, inflammation, fibrosis and increased actin expression, histopathologically (p < 0.05 for each). In this experimental steatohepatitis anti-TNF-alpha antibody decreased the levels of AST, ALT, TGF-beta(1) and plasma and tissue MDA (p < 0.05 for each). Moreover, inflammation, necrosis, actin expression and fibrosis decreased in anti-TNF-alpha group compared to placebo group (p < 0.05 for each). This study indicates that anti-TNF-alpha antibody is effective on necrosis, inflammation and fibrosis in the experimental model of non-alcoholic steatohepatitis, induced by MCD diet.
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PMID:The treatment with antibody of TNF-alpha reduces the inflammation, necrosis and fibrosis in the non-alcoholic steatohepatitis induced by methionine- and choline-deficient diet. 1806 56

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

Many plants found in nature have been used to treat various illnesses. One such plant is oregano (Kekik in Turkish). Health beneficial effects of carvacrol obtained from oregano oil have been shown scientifically. We have investigated the comparative effects of carvacrol in the liver of rats subjected to ischemia-reperfusion defect, with silymarin. To test the effects we formed four groups using male Wistar albino rats. Group I was control. The other three groups of animals were administered 60min prior to surgical operation single doses of physiological serum, carvacrol and silymarin, respectively. Group II, III and IV animal were subjected to 45min long liver ischemia and 60min reperfusion. Blood and tissue samples were collected for biochemical and histological analysis following the test. AST and ALT values obtained after biochemical analysis of the serums showed statistically significant difference in group II than the other three groups. A statistical evaluation of the serum AST levels among the groups II, III and IV showed that both groups III and IV which had no difference in between were significantly different in a positive way from group II (p<0.001). As to the serum ALT levels, difference between group II and group III (p<0.001) and group II and group IV (p<0.01) was found significant. No statistical difference was observed in groups I, III and IV for GSH, MDA and CAT levels of the liver. A statistical evaluation of the GSH level in group III and group IV was found to be significantly different from group II (p<0.001) without any difference between them. A similar evaluation for MDA and CAT levels among the revealed no difference between group III and group IV, however, group II showed difference with group II and group IV (p<0.05). Histological findings were in harmony with the biochemical results. We conclude that carvacrol protects the liver against defects caused by ischemia and reperfusion, and carvacrol is not hepatotoxic at the applied dosage.
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PMID:Effects of carvacrol on defects of ischemia-reperfusion in the rat liver. 1822 68

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

The aim of this study was to investigate the clinical, haematological, biochemical, lipid peroxidation, ultrasonographic and pathologic findings in hepatic coccidiosis induced by Eimeria stiedae in rabbits, and also to compare the treatment effects of both toltrazuril and ivermectin separately and in combination. In this study, 56 rabbits were divided into eight groups. The first group was designated as healthy control group. Rabbits were infected with 40.000 sporulated oocysts of E. stiedae. Groups 2, 3, 4, 5, 6, 7 and 8 were allocated as the infected control group, infected+toltrazuril-treated group, infected+ivermectin-treated group, infected+toltrazuril+ivermectin-treated group, non-infected+toltrazuril-treated group, non-infected+ivermectin-treated group, non-infected+toltrazuril+ivermectin-treated group, respectively. Haematocrit, Haemoglobin and MCV values as well as percentage of lymphocyte decreased in Groups 2 and 4 whereas leucocyte counts and percentage of granulocyte leucocyte increased. Serum GGT, ALT and AST activities increased but albumin value decreased. Plasma MDA concentrations increased whereas erythrocyte CAT, GSH-Px, and SOD activities decreased. Mean oocyst numbers in per gram faeces (epg values) increased in both groups during the study. Ultrasonographic examination revealed that the liver was enlarged and had hyperechogenic parenchyma. Bile ducts were dilated and hyperechogenic and the gall bladder was dilated. The livers of these animals were enlarged and typical macroscopic and microscopic findings of coccidiosis were present. Treatment with toltrazuril and toltrazuril+ivermectin combination were highly effective in reducing faecal oocyst output in infected rabbits. Haematological, biochemical and lipid peroxidation parameters and, ultrasonographic findings of the liver were close to control values for Groups 3 and 5. Necropsy of these animals showed no visible lesions related to hepatic coccidiosis although a few oocysts were detected in the bile duct epithelial cells.
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PMID:Eimeria stiedae: experimental infection in rabbits and the effect of treatment with toltrazuril and ivermectin. 1832 85

To study the effect of bicyclol on lipid disorder and liver damage induced by tetracycline in mice, mice were given (ig) bicyclol (75, 150, and 300 mg x kg(-1)) three times before or after administration of tetracycline (180 mg x kg(-1)). The contents of hepatic lipids, MDA and GSH, serum lipids and ALT/AST levels were measured 24 hours after the injection (ip) of tetracycline. The beta-oxidation rate of hepatic mitochondrial fatty acid and hepatic secretion of VLDL were also observed. Bicyclol (150 and 300 mg x kg(-1)) provided significant protection against fatty liver by inhibiting the elevation of hepatic TG and CHO, adjusting abnormal serum lipids, inhibiting the elevation of serum ALT, AST, and ameliorating the severity of pathological changes. Furthermore, bicyclol significantly accelerated the VLDL (TG) secretion and reversed the impairment of mitochondrial oxidation, resulting in the lipid homeostasis. The increase of MDA formation and depletion of GSH that reflect lipid peroxidation induced by tetracycline were also inhibited by bicyclol administration. The results indicated that the hepatoprotection of bicyclol was mostly due to the improvement on lipid oxidation and transportation as well as the inhibition of lipid peroxidation in tetracycline-intoxicated mice.
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PMID:[Protective effect of bicyclol against acute fatty liver induced by tetracycline in mice]. 1835 27

Ganoderma lucidum (GL), a traditional Chinese medicinal mushroom, has been widely used for the treatment of chronic hepatopathy of various etiologies. The hepatoprotective activity of peptides from Ganoderma lucidum (GLP) was evaluated against d-galactosamine (d-GalN)-induced hepatic injury in mice. GLP was administered via gavage daily for 2 weeks at doses of 60, 120 and 180 mg/kg, respectively. Control groups were given the same amount of physiological saline synchronously. Then the mice from d-GalN control and GLP-treated groups were treated with d-GalN (750 mg/kg) suspended in normal saline by intraperitoneal injection. d-GalN-induced hepatic damage was manifested by a significant increase in the activities of marker enzymes (AST, ALT) in serum and MDA level in liver (P<0.01), and by a significant decrease in activity of SOD and GSH level in liver (P<0.01). Pretreatment of mice with GLP reversed these altered parameters to normal values. The biochemical results were supplemented by histopathological examination of liver sections. The best hepatoprotective effects of GLP were observed after treatment with the dose of 180 mg/kg as it was evidenced from biochemical parameters and liver histopathological characters which were similar to those of normal control group. Results of this study revealed that GLP could afford a significant protection in the alleviation of d-GalN-induced hepatocellular injury.
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PMID:Hepatoprotective effects of Ganoderma lucidum peptides against D-galactosamine-induced liver injury in mice. 1840 49

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


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