Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.3.1.109 (AST)
 6,066 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Retrovirally induced immunosuppression may elevate the incidence of chemically induced cancers. A proposed hypothesis to explain this relationship is the increased free radical activity observed during retroviral infection and carcinogen activation. We previously found that vitamin E retarded growth of esophageal tumors accompanied by reductions of free radical products. This study investigated the contribution that retroviral immunosuppression has on esophageal cancer induced by the carcinogen N-nitrosomethylbenzylamine (NMBzA), and the response that increased levels of dietary vitamin E has on this induced carcinogenesis. Female C57BL/6 mice received NMBzA or vehicle (corn oil) i.p. weekly for 3 weeks. Then some of the mice were infected with LP-BM5 murine retrovirus and fed diets containing 30 IU vitamin E or 172 IU vitamin E/kg of diet. As an assessment of free radical activity, exhaled ethane was measured prior to killing the animals at 26 weeks. Esophagi from the various mice groups were assessed for size and frequency of tumors. Livers homogenates were analyzed for vitamins A and E, lipid fluorescence, conjugated dienes and malondialdehyde. Hepatic levels of vitamin A and E were decreased (P < 0.05) and indices of lipid peroxidation were greater (P < 0.05) in NMBzA-treated mice relative to controls. Lipid peroxidation and serum transaminases (ALT and AST) were greatest in mice given NMBzA and infected with the retroviruses. Incidence of esophageal tumors were also greatest in the NMBzA-treated, immunocompromised animals. Mice fed vitamin E-supplemented diets showed increased (P < 0.05) hepatic concentrations of vitamin E and vitamin A, decreased activities of serum transaminases, decreased indices of lipid peroxidation, and decreased size and frequency of esophageal tumors in both the immunocompromised and non-immunocompromised mice. These results suggest that vitamin E plays an antioxidant function that retards the incidence of esophageal cancers in immunocompromised and non-immunocompromised animals.
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PMID:Vitamin E protection against nitrosamine-induced esophageal tumor incidence in mice immunocompromised by retroviral infection. 133 Mar 43

The possible aggravation of liver injury by impaired cellular antioxidant function was investigated. A vitamin E-deficient diet (0.5 mg/kg alpha-tocopherol; control 100 mg/kg) significantly reduced rat liver alpha-tocopherol concentrations after 4 weeks (1.8 +/- 1.7 micrograms/g; control 34.4 +/- 2.4 micrograms/g, p < 0.001). The effects of copper loading (Cu, 3 g/kg diet); galactosamine (GalN, 0.85 g/kg i.p.); or carbon tetrachloride (CCl4, 10 mmol/kg i.p.) were examined. Serum aspartate transaminase activity was elevated slightly by vitamin E deficiency but not by hepatic copper accumulation. In vitamin E-replete (E+) and vitamin E-deficient (E-) rats, GalN or CCl4 caused a large and comparable elevation in serum AST and OCT activity. This effect on AST was markedly reduced by copper loading in vitamin E replete (E+) rats, but in E(-) rats copper had significantly less protective effect. Copper also diminished the OCT response to GalN in E+, though not E-, rats. A significant rise in total hepatic alpha-tocopherol content followed administration of GalN or CCl4 in both normocupric and copper-laden E(-) rats. Thus alpha-tocopherol deficiency (a) was not hepatotoxic per se; (b) failed to potentiate the toxicity of copper, GalN or CCL4; but (c) partially abolished the protection by copper against toxin-induced liver injury. Retention of hepatic alpha-tocopherol after liver damage may partly explain low serum vitamin E levels seen in clinical liver disease.
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PMID:Alpha-tocopherol deficiency fails to aggravate toxic liver injury but liver injury causes alpha-tocopherol retention. 148 10

In the companion paper we demonstrated that hepatic vitamin E in rats becomes depleted and extrahepatic pools of vitamin E are altered by treatment with 1,2-dibromoethane (DBE). Vitamin E depletion may be dependent upon initial steps of DBE metabolism that are either oxidative (cytochrome P450 dependent) or conjugative (glutathione transferase dependent). That the liver content of glutathione (GSH) and vitamin E, the plasma concentration of vitamin E, and the serum activities of AST and ALT may be influenced by cytosolic metabolism of DBE was assessed by comparison of findings from rats treated with either 1,2-dichloroethane (DCE) or 1-bromo-2-chloroethane (BCE). The extent of oxidative metabolism was diminished by the use of tetradeutero-DBE (d4-DBE), and the availability of GSH for conjugative metabolism was diminished by pretreatment of rats with L-buthionine-S,R-sulfoximine (BSO) prior to treatment with DBE. Our results indicate that neither DCE nor BCE provokes a liver vitamin E depletion in rats, that d4-DBE treatment hastens but does not enhance the observed hepatic vitamin E depletion by comparison to animals treated with an equimolar dose of DBE, and that BSO pretreatment prevented the hepatic vitamin E depletion observed from animals treated with DBE alone. These results indicate that hepatic vitamin E depletion is the unique sequelae to conjugation of GSH with DBE, and we suggest the reactive episulfonium ion intermediate or a macromolecular adduct of this ion derived from DBE may play a role in liver vitamin E depletion associated with exposure to DBE.
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PMID:Modification of hepatic vitamin E stores in vivo. III. Vitamin E depletion by 1,2-dibromoethane may be related to initial conjugation with glutathione. 189 41

Serum aminoterminal procollagen III peptide (PIIIP) was measured in 36 alcoholic subjects. There was a significant elevation of PIIIP in subjects with proven liver disease (median 17.5 ng/ml, n = 24) compared to those without liver disease (median 4.7 ng/ml, n = 12). Those subjects with raised serum transaminase values (AST) had elevated PIIIP values (median 13.7 ng/ml, n = 22) compared to those with normal transaminase values (median 3.7 ng/ml, n = 14). In those alcoholic subjects who were deficient in both selenium and vitamin E there was a significant elevation (p less than 0.01) of PIIIP values (median 26.4 ng/ml, n = 7) compared to subjects with normal levels (median 7 ng/ml, n = 11). Subjects deficient in selenium alone had PIIIP values in an intermediate range. Selenium and vitamin E, as important free radical scavengers, may protect the liver in alcoholic subjects from oxidative damage leading to hepatic fibrosis.
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PMID:Aminoterminal procollagen III peptide elevation in alcoholics who are selenium and vitamin E deficient. 395 42

Primary cultures of adult rat hepatocytes were incubated (6 to 96 hr) with 50 to 150 mmol/L ethanol, 0.5 mmol/L linoleate, 0.5 mmol/L palmitate, 0.5 mmol/L 4-methylpyrazole, 0 to 25 mumol/L vitamin E phosphate or selected combinations of these agents. Agent-dependent changes in liver cell viability (AST release and reduction of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and function (phospholipid peroxidation, hydrolysis, biosynthesis and triacylglycerol biosynthesis) were determined. The influence of ethanol on liver cell function and viability was dose and incubation time dependent. Short periods (24 hr or less) of exposure to 100 mmol/L ethanol increased liver cell triacylglycerol biosynthesis and phospholipid hydrolysis, peroxidation and biosynthesis without altering cell viability. However, longer periods (72 hr or more) of exposure to 100 or 150 mmol/L ethanol resulted in significant reductions (30% to 50%) in cell viability, function and phosphatidylcholine biosynthesis and content. The ethanol-dependent decreases in cell function and viability were potentiated by linoleate and reduced by vitamin E phosphate, palmitate and 4-methylpyrazole. These results suggest that ethanol-induced liver cell injury in vitro is not a result of ethanol per se, but factors such as acetaldehyde or oxyradicals produced as a consequence of ethanol metabolism. Therefore the incubation of cultured hepatocytes with ethanol may be an appropriate model in vitro for determining the mechanisms by which ethanol intake disrupts liver cell function in vivo.
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PMID:An in vitro model of ethanol-dependent liver cell injury. 827 54

Sixteen dairy cows were studied to assess the status of the natural antioxidant vitamin E and lipid peroxidation in their livers. Cows with liver failure (n = 7) showed clinical signs of a hepatic encephalopathy and had the following values of selected blood indices: AST > 80 U/l and GLDH > 15 U/l in serum, and venous plasma ammonia > 35 mmol/l. The control group (n = 9) consisted of dairy cows which were recovering from surgery (omentopexy) and were free of any health complications. Blood was analysed for alpha-tocopherol, aspartate aminotransferase, glutamate dehydrogenase, gamma-glutamyl transferase, total bilirubin, ammonia, cholesterol, albumin, free fatty acids, glucose, and beta-hydroxybutyrate. Alpha-tocopherol, triglyceride and malondialdehyde were measured in wet liver tissue. The cows with hepatic failure were clearly low in alpha-tocopherol and had significantly lower (P < 0.01) plasma alpha-tocopherol than the controls. Both liver triglycerides and MDA were higher (P < 0.05) in the cows with fatty livers. It is concluded that the cows with liver failure had an increase in the intensity of hepatic lipoperoxidative processes and a low antioxidative status, which should be taken into consideration in cases where treatment of the disease is proposed.
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PMID:A study of lipid peroxidation and vitamin E in dairy cows with hepatic insufficiency. 1039 80

Pentachlorophenol (PCP) is a pesticide used worldwide in industrial and domestic applications. It is used extensively as biocide and wood preservatives. Metabolic studies carried out in rodents and human liver homogenates have indicated that PCP undergoes oxidative dechlorination to form tetrachlorohydroquinone (TCHQ). Free radical catalyzed tissue injury is thought to play a fundamental role in human disease. In the present study, we examined the effects of PCP and TCHQ on the induction of lipid peroxidation and liver injury in rats. In addition, the cytotoxic dose, cell death mechanisms and related gene expressions induced by PCP and TCHQ were also determined for human hepatoma cell line (Hep G2). The results indicated that more toxic effects could be observed both in rats and human hepatoma cell line treated with TCHQ than its parent compound, PCP. Oxygen species may be involved in the mechanism of TCHQ intoxication since the urinary 8-epi-PGF2alpha and AST, ALT activities can be induced by TCHQ and attenuated by vitamin E treatment. Apoptosis features were found in cells treated with TCHQ but not PCP. TCHQ-induced cell damage may issue signals for the induction of HSPs, the decrease of the bcl/bax protein ratio and the decrease of CAS gene, whereas the PCP-induced damage may not.
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PMID:Oxidative stress and liver toxicity in rats and human hepatoma cell line induced by pentachlorophenol and its major metabolite tetrachlorohydroquinone. 1143 22

Our aim was to study the antioxidant and immunomodulatory effect of silibinin and vitamin E on the early postoperative course in rats that had undergone a partial hepatectomy (PHX). Male Wistar rats that were treated with silibinin (50 mg/b.w.kg i.p.) and/or vitamin E (500 mg/b.w.kg p.o.) were randomised to undergo 70% PHX. At 72 h after operation, Concanavalin A (Con-A) induced lymphocyte proliferation, and lipopolysaccharide (LPS) induced interleukin-1 (IL-1) mitogenicity and tumour necrosis factor-alpha (TNF-alpha) cytotoxicity were measured in the spleen. In addition, total free radical scavenger capacity of the liver was analysed. In PHX animals, Con-A induced lymphocyte proliferation was significantly decreased, and both LPS induced IL-1 and TNF-alpha activity were significantly increased as compared to Sham treated animals. Treatment with silibinin and vitamin E synergistically restored both lymphocyte proliferation (P<0.01) and cytokine activity (P<0.001) in PHX animals. In addition, silibinin and vitamin E synergistically (P<0.001) restored total hepatic free radical scavenger capacity as well as serum levels of AST and gammaGT, that were all markedly decreased in PHX animals. Our results suggest that preoperative treatment with silibinin and/or vitamin E modulates the cellular immunoresponse and restores impaired liver function following PHX, presumably through their antioxidant capacity. This may explain their beneficial effects on the postoperative course of liver repair.
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PMID:Effect of silibinin and vitamin E on restoration of cellular immune response after partial hepatectomy. 1153 68

HIV/AIDS is a multifactorial and multi-step disease. No single treatment against AIDS can save a patient. Our last report showed that vitamin A, vitamin E and beta-carotene were decreased while malondialdehyde (MDA) was increased. This report aims to evaluate biochemical and hematological parameters in HIV/AIDS patients in Chiang Mai, Thailand by holistic approaches. Sera from HIV/AIDS patients were examined for sugar, cholesterol, uric acid, total protein, albumin, urea, creatinine, AST, ALT, ALP, total/direct bilirubin, vitamin E, MDA, total antioxidant capacity (TAC), beta-carotene, complete blood cell counts, platelet count, CD4 count, prothrombin time, partial prothrombin time and soluble Fas (sFas). The results found that sFas levels in sera prior to holistic approach was not different from reference values and not significantly correlate with CD4 and absolute lymphocyte count. sFas could not serve as putative marker for CD4 destruction. After 3 months CD4 count, MDA, vitamin E and TAC did not change statistically. This approach had no effect on liver and kidney functions, red blood cell, white blood cell, platelet counts, and blood clotting factors. This presentation may be some alternative approaches to combat HIV infections and AIDS, leading to stabilize or extend survival time which should further be elucidated.
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PMID:Biochemical and hematological manifestations of HIV/AIDS in Chiang Mai, Thailand. 1194 6

The alcoholic liver disease usually causes overall immunological alterations which might be attributed to hepatic disease, to ethanol action, and/or to malnourishment. In the present study, efficacy of lecithin with vitamin-B complex to treat ethanol induced immunomodulatory activity was compared with the effect of lecithin alone and tocopheryl acetate (vitamin E). Ethanol (1.6 g/kg body wt/day for 12 weeks) exposure increased thiobarbituric acid reactive substance (TBARS) level, while decreased superoxide dismutase (SOD) activity and reduced glutathione (GSH) content in whole blood hemolysate of 8-10 week-old male BALB/c mice (weighing 20-30 g). The activities of transaminase (AST and ALT) enzymes, interleukin (IL)-10 and gamma interferon (IFN-gamma) elevated, while IL-2 and IL-4 reduced in mice serum due to ethanol exposure. These suggested that oxidative stress and immunomodulatory activities were interdependent and associated with ethanol induced liver damage. Lecithin treatment significantly reduced AST (32.44%), ALT (32.09%), IL-10 (25.63%) activities and TBARS content (12.76%) compared to ethanol treated group. However, lecithin with vitamin-B complex treatment, significantly reduced AST (62.83%); ALT (61.96%); IL-10 (35.88%); IFN-gamma (22.55%) activities and TBARS content (31.58%), while significantly elevated GSH content (36.49%) and SOD activity (61.21%). Tocopheryl acetate treatment significantly reduced AST (62.83%); ALT (61.54%); IL-10 (36.35%): IFN-gamma (23.28%) activities and TBARS content (35.84%). while significantly elevated GSH content (28.76%) and SOD activity (62.42%) compared to ethanol treated group. These findings persuasively argued that lecithin with vitamin-B complex was a new promising therapeutic approach in controlling ethanol induced immunomodulatory activities involving liver damage processes. Prevention of oxidative stress with correction of nutritional deficiency caused alteration in the ethanol-induced immunomodulatory activities and associated liver diseases.
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PMID:Effect of lecithin with vitamin-B complex and tocopheryl acetate on long-term effect of ethanol induced immunomodulatory activities. 1787 44


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