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)

The antioxidant activity of [N, N'-Bis (salicylidene) ethane-1, 2-diaminato] oxovanadium (IV) complex (VO-salen complex) was evaluated using different in vitro evaluating systems including superoxide anion (O(2)(-)) and hydrogen peroxide (H(2)O(2)) scavenging activities. In addition, the inhibitory effects of this compound on protein oxidation and inhibition of Fe(2+)/ascorbate-induced lipid peroxidation were studied using rat liver homogenate. In vitro results revealed that the VO-salen complex has strong inhibitory effects on protein oxidation and lipid peroxidation of the liver homogenate along with a concentration-dependent quenching of H(2)O(2) and O(2)(-) radicals. In an in vivo approach, hepatoprotective potential of the VO-salen complex against liver damages induced by CCl(4) treatment was also investigated. After intraperitoneal injection of CCl(4) to rats, various biochemical changes associated with liver injury and/or oxidative stress were measured. The results showed that the sera levels of ALT, AST, ALP and the content of hepatic thiobarbituric acid reactive substances (TBARS) were all increased and the glutathione (GSH) content and the hepatic superoxide dismutase (SOD) and catalase (CAT) activities were decreased in CCl(4)-treated rats. However, simultaneous treatment of rats with VO-salen (0.6 mg/kg) and CCl(4) significantly attenuated the sera levels of ALT, AST, ALP and the hepatic TBARS content. In addition, by VO-salen therapy, the hepatic SOD and CAT activities and the GSH content were all restored back almost to their normal levels. The liver damages were also significantly ameliorated as compared to the CCl(4)-treated rats. Based on these results, the VO-salen complex might be considered as an effective antioxidant and hepatoprotective agent suitable for further biological evaluation.
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PMID:Radical scavenging abilities and hepatoprotective effect of [N, N'-Bis (salicylidene) ethane-1, 2-diaminato] oxovanadium (IV) complex in CCl4-treated rats. 1964 Jun 93

Carvacrol (2-methyl-5-(1-methylethyl)-phenol) is a predominant monoterpenic phenol which occurs in many essential oils of the family Labiatae including Origanum, Satureja, Thymbra, Thymus, and Corydothymus species. This study was designed to investigate the hepatoprotective and antioxidant properties of carvacrol on D-galactosamine (D-GalN)-induced hepatotoxicity and oxidative damage in male albino Wistar rats. D-GalN hepatotoxic rats exhibited elevation in the activities of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, gamma-glutamyl transpeptidase, and lipidperoxidative markers such as thiobarbituric acid reactive substances (TBARS) and lipid hydroperoxides. Activities of enzymatic antioxidants (superoxide dismutase, catalase, and glutathione peroxidase) and the levels of non-enzymatic antioxidants (vitamin C, vitamin E, and reduced glutathione) in the plasma, erythrocytes, liver, and kidney decreased in the hepatotoxic rats. Oral administration of carvacrol for 21 days brought these parameters towards normal. The biochemical observations were supported by histological studies of rat liver and kidney tissues. These results suggest that carvacrol could afford a significant hepatoprotective and antioxidant effect against D-GalN-induced rats.
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PMID:Effect of carvacrol on hepatic marker enzymes and antioxidant status in D-galactosamine-induced hepatotoxicity in rats. 1965 Aug 54

Lambda-cyhalothrin is a synthetic pyrethroid insecticide used worldwide in agriculture, home pest control, protection of foodstuff and disease vector control. The objective of this study was to investigate the propensity of lambda-cyhalothrin (LTC) to induce oxidative stress, changes in biochemical parameters and enzyme activities in the kidney of male rats and its possible attenuation by Vitamin C (vit C). Renal function, histopathology, tissue malondialdehyde (MDA), protein carbonyl (PCO) levels, antioxidant enzyme activities and reduced glutathione (GSH) levels were evaluated. Exposure of rats to lambda-cyhalothrin, during 3 weeks, caused a significant increase in kidney MDA and protein carbonyl levels (p<0.01) as compared to controls. Co-administration of vitamin C was effective in reducing MDA and PCO levels. The kidney of LTC-treated rats exhibited severe vacuolations, cells infiltration and widened tubular lumen. The activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione-S-transferase (GST) were significantly decreased due to lambda-cyhalothrin exposure. Co-administration of vitamin C ameliorated the increase in enzymatic activities of aminotransferases (AST and ALT), lactate dehydrogenase (LDH), creatinine and urea levels and improved the antioxidant status. These data indicated the protective role of ascorbic acid against lambda-cyhalothrin-induced nephrotoxicity and suggested a significant contribution of its antioxidant property to these beneficial effects.
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PMID:Toxic effects of lambda-cyhalothrin, a synthetic pyrethroid pesticide, on the rat kidney: Involvement of oxidative stress and protective role of ascorbic acid. 1973 94

The effects of 80% ethanolic chlorella extracts (GPE) on carbon tetrachloride (CCl(4))-induced hepatic damage were investigated in Sprague-Dawley rats. The rats were orally treated with GPE (0.5 g/kg body weight) or silymarin (0.2 g/kg body weight) over four consecutive weeks with administration of CCl(4) (20% CCl(4), 0.5 ml/rat twice a week). The GPE had a significant protective effect against liver injuries, as well as oxidative stress induced by CCl(4), resulting in reduced lipid peroxidation and improved serum biochemical parameters such as aspartate aminotransferase and alanine aminotransferase. The reduced levels of glutathione, vitamin C, superoxide dismutase, and catalase in the CCl(4)-treated rats were significantly increased by treatment with GPE. Furthermore, the activity of GPE was comparable to the standard drug silymarin. In conclusion, chlorella may be useful as a hepatoprotective agent against chemical-induced liver damage in vivo.
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PMID:Hepatoprotection of chlorella against carbon tetrachloride-induced oxidative damage in rats. 1977 10

The present study investigates the protective effect of methanol extract of Ocimum gratissimum (MOEG) and Ocimum canum (MOEC) from Southern Africa on the oxidative stress induced by alcohol consumption. Male Wistar rats weighing 200-250 g were divided into six groups of six rats each as follows: the normal control group was administered distilled water, the ethanol control was administered ethanol (5 g/kg), and experimental groups EX1 and EX3 were fed ethanol (5 g/kg) plus MOEG and MEOC (100 mg/kg), respectively. Two other experimental groups, EX2 and EX4, were administered MEOG and MEOC (100 mg/kg), respectively, for 30 days. At the end of the experiment, rats were sacrificed, and blood was collected to assay thiobarbituric acid-reactive substances (TBARS), reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and vitamins E and C. Results indicated a significant reduction in the levels of TBARS, ALT, and AST and a significant increase in the levels of GSH and vitamins E and C. The level of vitamin E is greater with MOEG treatment, whereas the vitamin C level goes up with MOEC treatment. A marked improvement occurred in the activities of CAT and SOD in groups EX1 and EX3 compared to the levels with group EC. Thus the results indicated a significant protection by these extracts against ethanol-induced hepatotoxicity (P <or= .05). Again the groups that were treated with extracts only (EX2 and EX4) showed low levels of TBARS, ALT, and AST, which clearly indicates the extract had no toxic effects on hepatocytes. Comparison of results for these two Ocimum species showed no significant difference except in the levels of vitamins E and C with two treatments. Thus there is a possibility that O. canum might be participating through vitamin C and O. gratissimum through vitamin E.
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PMID:A comparative study of the antioxidant properties of two different species of Ocimum of southern Africa on alcohol-induced oxidative stress. 1985 83

Recent studies have shown that hormone replacement therapy (HRT) can exert regulatory affects on lipid and glucose homeostasis. It has been demonstrated that hyperglycemia also involving the formation of lipid peroxides, exert several biological effects that may contribute to the onset and progression of thyroid and kidney abnormalities of postmenopausal women Type 2 diabetes. Therefore, the aim of our study was to evaluate the effect of HRT, vitamin C and E (VCE) treatments on some plasma biochemical and hematological parameters and plasma thyroid hormone levels in postmenopausal women with or without diabetes. Oral HRT and VCE supplementation were compared with no HRT treatment in 40 non-diabetic postmenopausal women and 40 postmenopausal women with Type 2 diabetes mellitus, in a 6-week randomized prospective study. In the 20 women with diabetes who received oral HRT and the 20 women with diabetes who received HRT plus VCE, there was a significant fall in urea, uric acid, creatinine, total bilirubin, conjugated bilirubin, AST, ALT, LDH values. There was no significant change in red blood cell counts, total protein, albumin, sodium, potassium, hematocrit, hemoglobin and free thyrotoxine and triiodothyronine values in postmenopausal women with diabetes or treated with oral HRT and VCE. In conclusion, daily VCE and HRT administrations seem to produce significant improvement on biochemical parameters in the blood of postmenopausal women with Type 2 diabetes. The HRT and VCE supplementations may strengthen the antioxidant defense system and they may play a role in preventing kidney and liver diseases of postmenopausal women with Type 2 diabetes.
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PMID:Effects of hormone replacement therapy with vitamin C and E supplementation on plasma thyroid hormone levels in postmenopausal women with Type 2 diabetes. 1991 23

Mature male Wistar rats (weighing 300-320 g and each group six animals) were given malathion (27 mg/kg; 1/50 of the LD50 for an oral dose), vitamin C (200 mg/kg)+vitamin E (200 mg/kg), or both daily via gavage for 4 weeks. At the end of the fourth week, the malathion-treated group and the malathion plus vitamin-treated group both had significantly higher white blood cell (WBC) and thrombocyte counts than the control group. Compared to the control group, the two groups also had significantly higher serum total cholesterol, alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) levels, and significantly lower triglyceride and very low density lipoprotein (VLDL) levels. The malathion-treated rats also had significantly lower serum total protein and albumin levels, but the malathion plus vitamin-treated group did not differ from the control group in terms of these parameters. Moreover, concomitant vitamin treatment significantly normalized, at least partially, all of the other hematological and biochemical parameters that were altered by malathion. Light microscopic analyses revealed that both the malathion-treated and malathion plus vitamin-treated groups exhibited histopathological changes in liver tissues, although some pathological features were only observed in the malathion-treated group. Thus, vitamins C and E can reduce malathion hepatotoxicity, although the degree of protection they provide is limited.
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PMID:Malathion-induced hepatotoxicity in rats: the effects of vitamins C and E. 1994 25

Chrysin is a natural, biologically active compound present in many plants and possesses potent anti-inflammatory, anticancer and antioxidation properties. This work was designed to investigate the effect of chrysin, on the hepatoprotective efficacy in d-galactosamine-intoxication rats. d-galactosamine-induced toxicity was manifested by the elevation of serum hepatic marker enzyme activities (aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and gamma-glutamyl transpeptidase) and the lipid peroxidation process and by decreasing the antioxidant capacity of the plasma, erythrocyte and tissues. Treatment with chrysin (25, 50 and 100mg/kg body weight) decreased hepatic marker enzyme activities and lipid peroxidation products such as thiobarbituric acid reactive substances, lipid hydroperoxides and conjugated dienes, increased the activities of free-radical scavenging enzymes superoxide dismutase, catalase and glutathione peroxidase and the levels of non-enzymatic antioxidants reduced glutathione, vitamin C and vitamin E. These findings demonstrate that chrysin acts as a hepatoprotective and antioxidant agent against d-galactosamine-induced hepatotoxicity.
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PMID:Effect of chrysin on hepatoprotective and antioxidant status in D-galactosamine-induced hepatitis in rats. 2005 16

The present study evaluated the possible protective effects of selenium against atrazine-induced toxicity in the liver and reproductive system of rats. Atrazine administered to rats orally at a dose of 120 mg/kg caused an inhibition in the activity of glutathione-S-transferase and an increase in malondialdehyde formation in the liver, testis and epididymis. Superoxide dismutase decreased in the liver and testis but was increased in the epididymis. Furthermore, hepatic glutathione and lactate dehydrogenase activity increased while epididymal catalase, ascorbate content, hepatic aspartate aminotransferase and glutathione peroxidase activities in all the tissues decreased in the atrazine-treated animals. Hepatic, testicular and epididymal alanine aminotransferase activities were not affected by atrazine (p>0.05). Decreased epididymal and testicular sperm number, sperm motility, daily sperm production and increased number of dead and abnormal sperm were observed in atrazine-treated rats. Treatment of rats orally with selenium at a dose of 0.25 mg/kg did not prevent atrazine-induced changes in sperm characteristics and had no protective effects against atrazine-induced biochemical alterations in the testis and epididymis except testicular lactate dehydrogenase. Catalase activity and ascorbate contents were unchanged in these groups of animals. However, selenium effectively protected against atrazine-induced changes in biochemical indices in the liver. In rats treated with selenium alone, glutathione peroxidase in all the tissues, hepatic glutathione and superoxide dismutase, testicular lactate dehydrogenase activity and ascorbate content increased, while hepatic catalase activities decreased (p<0.05). Our data suggest that selenium effectively attenuated the toxic effects of atrazine-induced liver changes but not in the reproductive organs and sperms of rats. Selenium might therefore be useful in ameliorating oxidative stress in the liver.
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PMID:Selenium provides protection to the liver but not the reproductive organs in an atrazine-model of experimental toxicity. 2008 97

Excess hepatic iron generates reactive oxygen species that result in oxidative stress and oxidative damage to the liver. Vitamins have hitherto been considered to be a possible remedy. The aim of this study was to determine if high doses of delta-alpha-tocopherol supplementation in iron overload would ameliorate the oxidative stress. Four groups of 20 male Wistar albino rats were studied: group 1 (control) was fed normal diet, group 2 (Fe) 0.75% Ferrocene iron, group 3 (FV gp) 0.75% Ferrocene/delta-alpha-tocopherol (10x RDA), group 4 (V gp) normal diet/delta-alpha-tocopherol. After 12 months, serum iron, reduced glutathione, catalase, vitamin C, Oxygen Radical Absorbance Capacity, lipid peroxidation, 8-hydroxy-2'-deoxyguanosine (8-OHdG), aspartate transaminase (AST), and alanine transaminase (ALT) were measured. Vitamin C levels were: F gp = 5.04 +/- 0.09; FV gp = 5.85 +/- 0.13 (micromol/l) (p < 0.05). 8-hydroxy-2'-deoxyguanosine levels were: F gp = 143.6 +/- 6.4; FV gp = 179.2 +/- 18.2 (ng/ml) (p < 0.05). Oxidative liver damage, as determined by serum AST and ALT levels, was not attenuated by alpha-tocopherol. A positive correlation existed between vitamin C and 8-OHdG, suggesting possible delta-alpha-tocopherol toxicity.
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PMID:Possible adverse effect of high delta-alpha-tocopherol intake on hepatic iron overload: enhanced production of vitamin C and the genotoxin, 8-hydroxy-2'- deoxyguanosine. 2010 38


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