Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was designed to investigate the effect of Trolox, a hydrophilic analogue of vitamin E, on the alteration of vasoregulatory gene expression during hepatic ischemia and reperfusion (I/R). Rats were subjected to 60 min of hepatic ischemia in vivo. The rats were treated intravenously with Trolox (2.5 mg/kg) or the vehicle as a control 5 min before reperfusion. Liver samples were obtained 5 h after reperfusion for a RT-PCR analysis on the mRNA for the genes of interest. These mRNA peptides are endothelin-1 (ET-1), potent vasoconstrictor peptide, its receptor ET(A) and ET(B), vasodilator endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), heme oxygenase-1 (HO-1), tumor necrosis factor-alpha (TNF-alpha) and cyclooxygenase-2 (COX-2). It was seen that serum alanine aminotransferase and lipid peroxidation levels were markedly increased after I/R and Trolox significantly suppressed this increase. In contrast, the glutathione concentration decreased in the I/R group, and this decrease was inhibited by Trolox. ET-1 mRNA expression was increased by I/R, an increase which was prevented by Trolox. The mRNA levels for ET(A) receptor was significantly decreased, whereas ET(B) receptor transcript increased in the I/R group. The increase in ET(A) was prevented by Trolox. The mRNA levels for iNOS and HO-1 significantly increased in the I/R group and Trolox attenuated this increase. There were no significant differences in eNOS mRNA expression among any of the experimental groups. The mRNA levels for COX-2 and TNF-alpha significantly increased in I/R group and Trolox also attenuated this increase. Our findings suggest that I/R induces an imbalanced hepatic vasoregulatory gene expression and Trolox ameliorates this change through its free radical scavenging activity.
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PMID:Effect of Trolox on altered vasoregulatory gene expression in hepatic ischemia/reperfusion. 1502 26

Role of alpha-tocopherol (vitamin E), beta-carotene and/or their combination as antioxidants against the toxicity of fenvalerate on blood hematology, free radicals, biochemical parameters, and semen quality were studied in male rats. Fenvalerate (20 mg/kg BW), vitamin E (100 mg/kg BW), beta-carotene (10 mg/kg BW), and vitamin E plus beta-carotene (100 + 10 mg/kg BW, respectively) were given alone or in combination with fenvalerate. The tested doses were given to rats every other day for 30 days. Results obtained showed that fenvalerate significantly (P < 0.05) induced free radicals in plasma and brain and insignificantly in liver and testes. While, vitamin E, beta-carotene alone and/or in combination decreased the levels of free radicals in plasma, liver, testes, and brain. The activities of glutathione S-transferase (liver), alkaline phosphatase (plasma and liver), aspartate aminotransferase (plasma, liver, and testes) and alanine aminotransferase (plasma and liver) were significantly (P < 0.05) increased due to fenvalerate administration. The activity of acetylcholinesterase was significantly (P < 0.05) decreased in brain and plasma, while plasma glucose, urea, creatinine, and bilirubin concentrations were significantly (P < 0.05) increased in rats treated with fenvalerate. Also, results showed a significant (P < 0.05) alterations in plasma proteins, hematological parameters, body weight, and relative weights of organs. Sperm concentration and motility (%) were significantly (P < 0.05) decreased, while dead and abnormal sperm increased in rats exposed to fenvalerate. Vitamin E, beta-carotene alone and/or in combination did not cause any changes in the investigated parameters, but improved semen quality and minimized the toxic effect of fenvalerate. The obtained results demonstrated the beneficial influences of vitamin E, beta-carotene alone and/or in combination in reducing the harmful effects of fenvalerate.
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PMID:Role of alpha-tocopherol and beta-carotene in ameliorating the fenvalerate-induced changes in oxidative stress, hemato-biochemical parameters, and semen quality of male rats. 1518 33

The extensive use of alternative medicine products, herbal remedies, and vitamins in large doses has reached an all time high in the general public. Some agents are reported and advertised as immune stimulants and may interfere with patients suffering from immune modification, autoimmune diseases, or transplant recipients. In this report, we will present an investigation into the use of herbal remedies and vitamins in our liver transplant population. We performed an investigation using a questionnaire to determine the use of herbal products and vitamins in our liver transplant population. Medical records were reviewed for each liver transplant recipient that admitted to consuming herbal products or vitamins. Information collected included patient demographics, transplant related information, laboratory tests, outcomes, and herbs or vitamin products used. A total of 290 patients completed and returned the questionnaire. We found 156 admitting to taking more than a standard multivitamin and/or an herbal remedy. All patients were treated with steroids for allograft rejection and experienced a recurrence of amino transaminases following the removal of steroids. Further investigation into dietary supplements using a patient questionnaire form revealed that nearly 50% of patients admitted to using vitamins following transplantation, while 19% used herbal remedies combined with vitamins, most admitting to silymarin. One recipient was ingesting colostrum and required admission for the management of allograft rejection, while 5 patients had consumed large amounts of echinacea or CoEnzyme Q-10 and experienced elevations in their transaminases that resolved with discontinuation of the herb. The review also identified 4 patients with primary biliary cirrhosis and with transaminase elevation (mean values of aspartate aminotransferase and alanine aminotransferase levels of 88 and 95, respectively). All recipients were consuming vitamins, in particular high doses of vitamin E (tocopherol), more than 1 gram per day. All of the transplant recipients were instructed to discontinue all vitamin E products and the amino transaminases resolved over the following 30 to 60 days. In conclusion, this information reveals that a significant proportion of our liver transplant recipients consume herbal remedies. The results of this report suggest that transplant teams need to question each recipient about the use of herbal and vitamin remedies and educate them regarding the potential hazards.
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PMID:Consumption of dietary supplements in a liver transplant population. 1563 45

Hepatotoxic substances such as aflatoxin B1 (AFB1) produce free radical reactions during biotransformation damage to liver cells. Vitamins C and E are important natural antioxidants suppressing free radicals. This study investigated the effects of vitamins C and E on liver enzymes and other biochemical parameters in rabbits experimentally exposed to AFB1. The first group was control and fed the diet with dimethyl sulfoxide; the second group received 0.1 mg AFB1/kg diet; the third group received vitamin C (100 mg L-ascorbic acid/kg diet); the fourth group received vitamin E (100 mg alpha-tocopherol/kg diet); and the fifth group received vitamin C+vitamin E (100 mg L-ascorbic acid/kg diet+100 mg alpha-tocopherol/kg diet). Diets of the second, third, fourth and fifth groups were mixed with 0.1 mg AFB/kg diet) and feedings were continued for 10 w. Levels of aspartate transaminase, alanine transaminase, alkaline phosphatase, creatine phosphokinase and lactate dehydrogenase after receiving AFB1 were significantly increased, while activities of aspartate transaminase, alanine transaminase, amylase, creatine phosphokinase and lactate dehydrogenase in groups receiving AFB1 + vitamins C, E or C+E were significantly lower than that of the AFB1-alone group. Although of the activity of alkaline phosphatase increased with AFB1 exposure, it decreased with vitamin C administration. Levels of urea, triglyceride, cholesterol and albumin were affected by AFB1 and AFB1+vitaminC. AFB1 affected some liver enzymes and other biochemical parameters, but vitamins C, E and C+E partially prevented an increase in these liver enzymes and some the biochemical parameters induced by AFB1.
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PMID:Effects of vitamin C and E on liver enzymes and biochemical parameters of rabbits exposed to aflatoxin B1. 1530 90

Cadmium is a well-known human carcinogen and a potent nephrotoxin. Lipid peroxidation is involved in cadmium-related toxicity. Vitamin E and beta-carotene are effective antioxidants and free radical scavengers. Therefore, the present study was carried out to investigate the potential protective effects of vitamin E and beta-carotene alone or in combination against cadmium (Cd) toxicity. Cadmium chloride (CdCl2, 5 mg/kg BW, 1/15 LD50), vitamin E (100 mg/kg BW), beta-carotene (10 mg/kg BW), and vitamin E with beta-carotene (100 + 10 mg/kg BW, respectively) were orally administered by gavage alone or in combination. The tested doses were given to rats every other day (15 times). Results obtained showed that CdCl2 significantly (P < 0.05) induced free radicals in plasma, liver and brain. The activities of glutathione S-transferase (GST) (plasma and liver), alkaline phosphatase (AlP) (plasma and liver), aspartate aminotransferase (AST), alanine aminotransferase (ALT) (liver) and acetylcholinesterase (AChE) (plasma and brain) were significantly (P < 0.05) decreased due to CdCl2 administration, whereas, the activities of AST and ALT were increased in plasma. Treatment with CdCl2 caused a significant (P < 0.05) increase in glucose, urea, creatinine and bilirubin in plasma. On the other hand, results showed that CdCl2 significantly (P < 0.05) decreased plasma total protein (TP), albumin (A), blood hemoglobin (Hb), total erythrocytic count (TEC) and packed cell volume (PCV), while total leukocyte count (TLC) increased. Treatment with CdCl2 caused a significant (P < 0.05) decrease in sperm concentration, motility (%), weight of testes and epididymis, and increase in dead and abnormal sperm. Results demonstrated the beneficial influences of vitamin E, -carotene alone and/or in combination in reducing the harmful effects of CdCl2.
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PMID:Cadmium-induced changes in lipid peroxidation, blood hematology, biochemical parameters and semen quality of male rats: protective role of vitamin E and beta-carotene. 1530 3

Aluminium has the potential to be neurotoxic in humans and animals, and is present in many manufactured foods and medicines and is also added to drinking water for purification purposes. Therefore, the present study was carried out to investigate (1) the alterations in biochemical parameters, free radicals and enzyme activities induced by aluminium chloride (AlCl3) in plasma and different tissues of male rats, and (2) the role of vitamin E (VE) and selenium in alleviating the negative effects of aluminium. VE plays an important role as an antioxidant and is consequently expected to protect tissues from damage caused by reactive oxygen metabolites. Selenium is also generally recognized to be a trace mineral of great importance for human health, protecting the cells from the harmful effects of free radicals. Seven rats per group were assigned to one of six treatment groups: 0 mg VE, 0 mg Se and 0 mg AlCl3/kg body weight (BW) (control); 100 mg VE/kg BW; 200 microg Se kg BW; 34 mg AlCl3/kg BW (1/25 LD50); 34 mg AlCl3 plus 100 mg VE/kg BW; 34 mg AlCl3 plus 200 microg Se/kg BW. Rats were orally administered their respective doses every other day for 30 days. Evaluations were made for lipid peroxidation, enzyme activities and biochemical parameters. Results obtained showed that AlCl3 significantly (p<0.05) induced free radicals (thiobarbituric acid-reactive substances) and decreased the activity of glutathione S-transferase (GST) and the levels of sulphydryl groups (SH groups) in rat plasma, liver, brain, testes and kidney. Aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, acid phosphatase, and phosphorylase activities were significantly decreased in liver and testes due to AlCl3 administration, while the activities of these enzymes were significantly increased in plasma. In addition, plasma, liver, testes and brain lactate dehydrogenase activities were significantly increased. On the contrary, the activity of acetylcholinesterase was significantly decreased in brain and plasma. Al treatment caused a significant decrease in plasma total protein (TP), albumin and total lipids (TL), and increased the concentrations of glucose, urea, creatinine, bilirubin and cholesterol. VE or Se alone significantly decreased the levels of free radicals, TL, cholesterol, urea and bilirubin, and increased the activity of GST, and SH groups, TP and albumin, while the rest of the tested parameters were not affected. VE or Se in combination with Al partially or totally alleviated its toxic effects on the studied parameters. In conclusion, VE and Se have beneficial effects and could be able to antagonize Al toxicity.
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PMID:Antioxidant effect of vitamin E and selenium on lipid peroxidation, enzyme activities and biochemical parameters in rats exposed to aluminium. 1548 71

Cyclophosphamide (CP), one of the most widely prescribed antineoplastic drugs could cause a lethal cardiotoxicity. The present study is aimed at evaluating the role of DL-alpha-lipoic acid (LA) in oxidative cardiac damage induced by CP. Adult male Wistar rats were divided into four treatment groups. Two groups received single intraperitoneal injection of CP (200 mg/kg BW) to induce cardiotoxicity, one of these groups received LA treatment (25 mg/kg BW for 10 days). A vehicle treated control group and a LA drug control were also included. Cardiotoxicity, evident from increased activities of serum creatine phosphokinase, lactate dehydrogenase, aspartate transaminase and alanine transaminase in CP administered rats, was reversed by LA treatment. CP administered rats showed abnormal levels of enzymic (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase) and non-enzymic antioxidants (glutathione, vitamin C and vitamin E) along with high malondialdehyde levels. However, normalized lipid peroxidation and antioxidant defenses were reported in the LA treated rats. These findings highlight the efficacy of LA as a cytoprotectant in CP induced cardiotoxicity.
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PMID:Protective effect of DL-alpha-lipoic acid on cyclophosphamide induced oxidative cardiac injury. 1560 58

We investigated the effect of raxofelast on lipid peroxidation inhibition in mice exposed to chronic ethanol. Female C57BL/6 mice were fed a modified Lieber-DeCarli liquid ethanol (ETOH) or control diet (sham ETOH) for up to 14 days. Animals were assigned to receive either raxofelast (20 mg/kg/day i.p.) or its vehicle (DMSO:NaCl 0.9% 1:1, v:v; 1 ml/kg i.p.). Serum alanine aminotransferase (ALT), plasma and liver triglyceride levels, hepatic malondialdehyde (MDA), reduced glutathione (GSH) concentrations, liver gene expression of Toll-like receptor-4 (TLR-4), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) and intercellular adhesion molecule-1 (ICAM-1) were studied at the end of the study. A histological evaluation of liver damage was also carried out. Raxofelast, an analog of vitamin E, blunted the increased hepatic nuclear factor-kappaB activity, reduced serum ALT, plasma and liver triglycerides, lowered hepatic MDA levels, prevented liver GSH depletion and decreased TLR-4, TNF-alpha, IL-6 and ICAM-1 hepatic gene expression. Furthermore raxofelast ameliorated liver damage. Our results suggest that raxofelast blunts the inflammatory cascade and organ damage during chronic ethanol exposure.
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PMID:Protective effects of antioxidant raxofelast in alcohol-induced liver disease in mice. 1562 48

The oxidative stress induced by chronic ethanol consumption, particularly in concert with the aging process, has been implicated in changes in the structure and functions of liver cell components including membrane phospholipids. To counteract such changes, particularly those resulting from lipid peroxidation, antioxidants may be applied. Green tea contains large amounts of polyphenols, mainly catechins, which possess antioxidant properties. The aim of this study was to estimate the efficacy of green tea's influence on the physicochemical and biochemical properties of the rat liver as affected by the aging process and/or chronic ethanol intoxication. Several methods were used to evaluate this effect. Antioxidant properties were evaluated by vitamin E and antioxidant status determination. The liver trigliceride and cholesterol levels were also estimated. The extent of lipid peroxidation was determined by measuring the level of lipid peroxidation products as thiobarbituric reactive substances (TBARS). The surface charge density of the rat liver cells was measured using electrophoresis. The concentration of the marker enzymes of liver damage (alanine aminotransferase and aspartate aminotransferase) in the blood serum was also evaluated. Relative to the controls, aging was found to cause a decrease in the liver's antioxidant abilities and provoke an increase in the level of lipid peroxidation; it also increased the surface charge density of the rat liver cell membrane. Ethanol significantly aggravated these changes. This might have resulted in the liver cell membrane damage visible as a leak of alanine aminotransferase and aspartate aminotransferase into the blood. The ingestion of green tea with ethanol partially prevented these aging and/or ethanol-induced changes. Long-term drinking of green tea partially prevents the changes in the structure and function of the cell membrane caused by chronic ethanol intoxication.
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PMID:Green tea modulation of the biochemical and electric properties of rat liver cells that were affected by ethanol and aging. 1564 93

Carbon tetrachloride feeding (3.2g/kg/72hr) for one month increased significantly the serum and tissue lipid profile and deranged the enzyme levels viz; alkaline phosphatase, alanine transaminase, aspartate transaminase, glutathionze reductase, HMGCoA reductase, catalase, gluc.6.PDH and malic enzyme in rats. Simultaneously the lipid peroxidation level in liver was also raised. On administration of garlic oil and its major nonpolar fraction (NPFGO) and a flavonoid isolated from the bark of Ficus bengalensis Linn, viz; leucopelargonin derivative respectively to different groups(100mg/kg/day) the deleterious effects of CCl4 were significantly ameliorated. The liver damage by CCl4 was satisfactorily prevented by these samples as effectively as Vit. E (50 mg/kg/day). The results prove that important nutraceuticals (phytonutrients) like bioflavonoids and theols i.e. allylic sulphide rich fractions give protection from toxins like CCl4. The order of beneficial effects of the drugs are Leucopelargonin > NPFGO > Garlic oil and their effects are comparable to that of vitamin E used at a minimal dose.
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PMID:Nutraceutical effects of garlic oil, its nonpolar fraction and a Ficus flavonoid as compared to vitamin E in CCl4 induced liver damage in rats. 1590 Sep 9


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