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:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increased oxidative stress and antioxidant deficit have been suggested to play a major role in adriamycin induced cardiomyopathy and congestive heart failure due to multiple treatments with adriamycin. In this study the cardio protective effect of Centella asiatica on myocardial marker enzymes and antioxidant enzymes in adriamycin induced cardiomyopathy was investigated in rats. The rats administered with adriamycin (2.5 mg/kg body wt, i.p) caused myocardial damage that was manifested by the elevation of serum marker (LDH, CPK, GOT and GPT) enzymes and showed significant changes in the antioxidant enzymes (SOD, CAT, GPx, GST). Pre-co-treatment with Centella asiatica(200 mg/kg of body wt/oral) extract significantly prevented these alterations and restored the enzyme activities to near normal levels. These findings demonstrate the cardio protective effect of Centella asiatica on antioxidant tissue defense system during adriamycin induced cardiac damage in rats.
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PMID:Protective effect of Centella asiatica on antioxidant tissue defense system against adriamycin induced cardiomyopathy in rats. 1555 70

Mercury is a highly toxic metal which induces oxidative stress. Superoxide dismutases, catalase, and glutathion peroxidase are proteins involved in the endogenous antioxidant defence system. In the present study rats were administered orally, by gavage, a single daily dose of HgCl2 for three consecutive days. In order to find a relation between the proteins involved in the antioxidant defence and mercury intoxication, parameters of liver injury, redox state of the cells, as well as intracellular protein levels and enzyme activities of Mn-dependent superoxide dismutase (MnSOD), Cu-Zn-dependent superoxide dismutase (CuZnSOD), catalase, and glutathione peroxidase (GPx) were assayed both in blood and in liver homogenates. HgCl2 at the doses of 0.1 mg/kg produced liver damage which that was detected by a slight increase in serum alanine aminotransferase and gamma glutamyl transferase. Hepatic GSH/GSSG ratio was assayed as a parameter of oxidative stress and a significant decrease was detected, as well as significant increases in enzyme activities and protein levels of hepatic antioxidant defence systems. Changes in both MnSOD and CuZnSOD were parallel to those of liver injury and oxidative stress, while the changes detected in catalase and GPx activities were progressively increased along with the mercury intoxication. Other enzyme activities related to the glutathione redox cycle, such as glutathione reductase (GR) and glucose-6-phosphate dehydrogenase (G6PDH), also increased progressively. We conclude that against low doses of mercury that produce a slight oxidative stress and liver injury, the response of the liver was to induce the synthesis and activity of the enzymes involved in the endogenous antioxidant system. The activities of all the enzymes assayed showed a rapidly induced coordinated response.
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PMID:Endogenous antioxidant defence system in rat liver following mercury chloride oral intoxication. 1597 96

The blood alcohol level cycle (BALC) of the intragastric tube feeding model first described by Tsukamoto et al., has three separate essential mechanistic components. The first is the requirement for an intact functioning thyroid. The evidence for this is that propylthiouracil or severance of the pituitary stalk completely prevents the cycle. What happens instead of the cycle is that the blood alcohol level rises to a lethal level when ethanol is given continuously at a dose of 11 g/kg/day by stomach tube. When excess thyroid hormone is given orally it markedly attenuates the cycle because it interferes with the changes in the level of thyroid hormone during the cycle. The second component is norepinephrine. Catecholamines are markedly elevated at the peaks of the cycle. Both propranolol and phenoxybenzamine, which are beta- and alpha-blockers, prevent the cycle. Also, when catecholamines are fed in excess in the form of ephedrine, the cycle is eliminated. The third element essential to the cycle is the generation of NAD to support the oxidation of alcohol by alcohol dehydrogenase. When complex I (NADH dehydrogenase) of the mitochondrial electron transport chain is inhibited by feeding rotenone, the cycle is totally eliminated and blood alcohol levels remain constant at 200 mg/%. Thus NADH increases and NAD decreases at the peak of the cycle. Without the fluxuation of NAD, ADH activity cannot fluctuate during the cycle and the cycle is prevented. The significance of the BALC in the understanding of alcohol liver disease pathogenesis is that there's a marked difference in the gene expression and liver toxicity when the peaks and troughs of the cycle are compared. The expression of 1000+ genes is either two-fold up or down regulated as determined by microarray analysis. At the peaks there is increased liver pathology, especially inflammatory changes in the liver associated with an increase of iNOS expression. The genes responsive to hypoxia inducible factor 1alpha (HIF1alpha) regulation are increased including the expression of erythropoietin, adrenomedullin and adrenergic receptor alpha 1a and d. The expression of prolyl hydroxylase, which destabilizes HIF1alpha, increases when the BAL drops to low levels during the cycle. The level of oxygen, as measured on the surface of the liver, is decreased at the peaks, compared to control livers. The NADH/NAD ratio is markedly increased and ATP levels are markedly decreased at the BAL peaks. Also, endotoxin in the blood is very high at the peaks and very low at the troughs. When the blood alcohol levels fall during the cycle, there is an increase in ALT, suggesting that reoxygenation from the hypoxic state at the peaks causes an ischemic reperfusion injury-like lesion in the liver. At this time there is also an increase in expression of many important enzymes such as manganese SOD. Genes such as c-fos and CTGF are increased in expression. These contrasting findings at the peaks and troughs indicate that the blood alcohol levels, which fluctuate up and down, change the gene expression and the pathology of the liver.
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PMID:The pathogenesis and significance of the urinary alcohol cycle in rats fed ethanol intragastrically. 1634 1

This study examined the effects of celecoxib on hepatic ischemia/reperfusion (I/R) injury in rats. A total of 40 male Sprague-Dawley rats weighing 190-210g were randomized into 4 groups of 10: (1) controls: data from unmanipulated animals; (2) sham group: rats subjected to the surgical procedure, except for liver I/R, and given saline; (3) I/R group: rats that underwent liver ischemia for 1h followed by reperfusion for 45min; (4) I-R/Celecoxib group: rats pretreated with celecoxib (3mgkg(-1), i.p.) 40min before liver I/R. Tc-99m sulfur colloid images were used to measure the uptake ratio and perfusion index. Liver tissues were taken to determine SOD, CAT, GSH-Px, and MDA levels and for biochemical and histological evaluation. The plasma ALT, AST, GGT, and LDH activities were higher in group 3 than in group 4. The uptake ratio was significantly lower in group 3 compared to groups 1, 2, and 4. In addition, in group 4, the uptake ratio and perfusion index were also significantly higher compared to group 3. MDA values and the hepatic injury score decreased, while the SOD, CAT, and GSH-Px values increased in group 4 compared to group 3. In group 3, hepatocytes were swollen with marked vacuolization. Group 4 showed well preserved liver parenchyma with hepatocytes arranged radially around the central vein; there were regular sinusoidal structures with normal morphology without any signs of congestion. We showed that celecoxib has beneficial effects in hepatic I/R injury and may protect the liver.
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PMID:The effect of celecoxib, a selective COX-2 inhibitor, on liver ischemia/reperfusion-induced oxidative stress in rats. 1638 42

Studies on the lipid peroxidation and antioxidant changes and their significance during myocardial injury have provided a new insight into the pathogenesis of heart disease. The heart failure subsequent to myocardial infarction may be associated with an antioxidant deficit as well as increased myocardial oxidative stress. The present study was designed to evaluate the effect of the combination of ferulic acid and ascorbic acid on antioxidant defense system and lipid peroxidation against isoproterenol (ISO)-induced myocardial infarction in rats. Induction of rats with isoproterenol (150 mg/kg body weight daily, i.p.) for 2 days resulted in a marked elevation in lipid peroxidation, serum marker enzymes (LDH, CPK, GOT, and GPT), and a significant decrease in activities of endogenous antioxidants (SOD, GPx, GST, CAT, and GSH). Pre-co-treatment with the combination of ferulic acid (20 mg/kg body weight/day) and ascorbic acid (80 mg/kg body weight/day) orally for 6 days, significantly attenuated these changes when compared to the individual treatment groups. Histopathological observations were also in correlation with the biochemical parameters. Thus, ferulic acid and ascorbic acid significantly counteracted the pronounced oxidative stress effect of ISO by the inhibition of lipid peroxidation, restoration of antioxidant status, and myocardial marker enzymes levels. In conclusion, these findings indicate the synergistic protective effect of ferulic acid and ascorbic acid on lipid peroxidation and antioxidant defense system during ISO-induced myocardial infarction and associated oxidative stress in rats.
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PMID:Synergistic interactions of ferulic acid with ascorbic acid: its cardioprotective role during isoproterenol induced myocardial infarction in rats. 1644 96

The anti-diabetic and antioxidative effect of amaranth grain (AG) and its oil fraction (AO) was studied in streptozotocin-induced diabetic rats. Male Sprague-Dawley rats were divided into four groups after induction of STZ-diabetes: normal control; diabetic control; diabetic-AG supplement (500 g kg(-1) diet); diabetic-AO supplement (100 g kg(-1) diet) and fed experimental diets for 3 weeks. Serum glucose, insulin, activities of serum marker enzymes of liver function and liver cytosolic antioxidant enzymes were measured. The AG and AO supplement significantly decreased the serum glucose and increased serum insulin level in diabetic rats. Serum concentration of liver function marker enzymes, GOT and GPT, were also normalized by AG and AO treatment in diabetic rats. Liver cytosolic SOD and GSH-reductase activities were significantly increased, and catalase, peroxidase and GSH-Px activities were decreased in diabetic rats. AG and AO supplement reverted the antioxidant enzyme activities to near normal values. Hepatic lipid peroxide product was significantly higher, and GSH content was decreased in diabetic rats. However, AG and AO supplement normalized these values. Our data suggest that AG and AO supplement, as an antioxidant therapy, may be beneficial for correcting hyperglycaemia and preventing diabetic complications.
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PMID:Antioxidative and anti-diabetic effects of amaranth (Amaranthus esculantus) in streptozotocin-induced diabetic rats. 1663 92

Alanine aminotransferase (AlaAT, EC 2.6.1.2) is an enzyme that is induced under anaerobic conditions in cereal roots. In barley (Hordeum vulgare L.) roots, there are a number of isoforms of AlaAT. We have identified the anaerobically induced isoform and have purified it to homogeneity. The isolation procedure involved a two-step ammonium sulfate precipitation, gel filtration, ion-exchange chromatography, and chromatofocusing. The enzyme was purified approximately 350-fold to a specific activity of 2231 units/milligram protein. The apparent molecular masses of the native and sodium dodecyl sulfate-denatured AlaAT proteins are 97 and 50 kilodaltons, respectively, indicating that the native enzyme is probably a homodimer. AlaAT has a number of interesting characteristics when compared with other plant aminotransferases. AlaAT does not require the presence of pyridoxyl-5-phosphate to retain its activity, and it appears to be very specific in the reactions that it will catalyze.
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PMID:Purification and characterization of an anaerobically induced alanine aminotransferase from barley roots. 1666 68

Cholestasis-induced liver injury during bile duct obstruction causes an inflammatory response and this inflammatory process may be an important source of tissue injury. We hypothesized that NF-kappaB inhibition would decrease liver injury in a rat model of extrahepatic biliary obstruction. A total of 40 female rats of Sprague-Dawley strain were allocated to four groups. First group was sham operated control. The second group underwent common bile duct ligation (BDL) and was monitored for 10 days. Third group of rats underwent BDL and received pyrrolidine dithiocarbomate (PDTC) at a dose of 100 mg/kg/day intraperitoneally. Fourth group underwent BDL and received sulfasalazine at a dose of 100 mg/kg b.w. Both inhibitors were administered once a day throughout last 7 days of the experimental period. Rats were terminated 10 days after sham operation or BDL. Aspartate aminotransferase, alanine aminotransferase, gamma-glutamil transpeptidase, and tumor necrosis factor-alpha levels were elevated in the BDL group as compared to the control group, while this increase was significantly decreased by treatment with PDTC and sulfasalazine (P < 0.05). Hepatic GSH, SOD and catalase levels were significantly depressed by BDL, but were elevated back to control levels in NF-kappaB inhibitor-treated BDL groups. Increases in tissue free radical and MDA levels and MPO activity due to BDL were reduced back to control levels by NF-kappaB inhibitor treatment (P < 0.05). Similarly histological damage in the BDL rats was reduced by treatments. These results indicate that inhibitors of NF-kappaB activity such as PDTB and sulfasalazine exert a therapeutic effect on cholestatic liver injury in rats with BDL through anti-inflammatory and antioxidant actions.
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PMID:The NF-kappaB inhibitors attenuate hepatic injury in bile duct ligated rats. 1683 Jan 61

The study was aimed at evaluating the antioxidant activity of alcoholic extract of Cassia siamea Lam. (Fabaceae) flowers. The extract was found to contain a large amount of polyphenols and also exhibited an immense reducing ability. At a concentration of 250 microg/ml, 96% of DPPH radicals and at 500 microg/ml, 42.7, 32.7 and 64.5% of O2-, H2O2 and NO respectively could be scavenged by C. siamea flower extract. The extract also inhibited OH radical induced oxidation of protein (BSA) and LPO in murine hepatic microsomes. The determination of metal chelating capacity of the extract indicated chelating of metal ions (Fe2+) to be a putative mechanism implicated in the inhibition of OH radical-induced BSA oxidation and LPO. C. siamea flower extract also exhibited a significant antioxidant activity in acute oxidative tissue injury animal model constituted by CCl4 induced hepatotoxicity. Oral administration of the extract at a dose of 50-150 mg/kg of body weight significantly protected from CCl4 induced elevation in AST and ALT in the serum, elevation in hepatic LPO, depletion of hepatic GSH and decrease in the activities of hepatic antioxidant enzymes: SOD, CAT and GPX. The extract also protected against histopathological changes produced by CCl4 such as necrosis, fatty changes, ballooning degeneration, etc. The data obtained in the present study suggests that the alcoholic extract of C. siamea flowers have potent antioxidant activity against free radicals, prevent oxidative damage to major biomolecules and afford significant protection against oxidative damage in the liver.
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PMID:Evaluation of antioxidant activity of Cassia siamea flowers. 1684 7

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


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