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)

The preventive effect of neutropenia on carbon tetrachloride (CCl4)-induced hepatotoxicity was examined in rats. In rats treated once with CCl4 (1 ml kg(-1), i.p.), the serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), indices of liver cell damage, and the hepatic activity of myeloperoxidase (MPO), an index of tissue neutrophil infiltration, increased at 6 h after the intoxication and further increased at 24 h. The liver of CCl4 -treated rats showed an increase in the concentration of thiobarbituric acid reactive substances (TBARS), an index of lipid peroxidation, and decreases in superoxide dismutase (SOD) activity and reduced glutathione (GSH) concentration at 6 h after the intoxication followed by a further increase in TBARS concentration and further decreases in SOD activity and GSH concentration at 24 h with increased xanthine oxidase (XO) activity at 24 h. Neutropenic treatment with anti-rat neutrophil antiserum (2 ml kg(-1), i.p.) at 0.5 h after CCl4 intoxication attenuated the increases in serum ALT and AST activities and hepatic MPO activity and TBARS concentration and the decreases in hepatic SOD activity and GSH concentration found at 6 and 24 h after CCl4 intoxication and the increase in hepatic XO activity found at 24 h after the intoxication. This neutropenia reduced the necrotic and degenerative changes with inflammatory cell infiltration in the liver cell of CCl4 -treated rats. These results indicate that neutropenia prevents CCl4 -induced hepatotoxicity in rats by attenuating the disruption of hepatic reactive oxygen species metabolism mediated by neutrophils accumulating in the liver tissue.
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PMID:Preventive effect of neutropenia on carbon tetrachloride-induced hepatotoxicity in rats. 1627 9

In the liver tissue of newborn mice, xanthine oxidase activity is very low during the first 7 to 14 days of life. Infection of mice with several different viruses prematurely induced xanthine oxidase activity 2- to 10-fold in the liver tissue. Generally, overt signs of illness appeared after xanthine oxidase induction; however, some viruses induced the enzyme activity without causing morbidity or deaths. The elevated enzyme activity could not be correlated with alteration of either lactate dehydrogenase or glutamate-pyruvate transaminase. Likewise, there were no histological changes in the livers of infected animals when xanthine oxidase levels were abnormally elevated. These observations suggest that measurement of xanthine oxidase may be an effective method for the detection of subclinical or inapparent viral infections in either naturally infected newborn mice or in newborn mice inoculated with suspected virus-containing materials.
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PMID:Induction of xanthine oxidase by virus infections in newborn mice. 1655 59

Tannic acid, present in almost every food derived from plants, has been widely investigated as a chemopreventive agent because, apart from its use as a food additive, pharmacological studies have demonstrated its many health-promoting properties. In this study, we show the modulatory effect of tannic acid on 2-acetylaminofluorene (2-AAF)-mediated hepatic oxidative stress and cell proliferation in rats. 2-AAF (50 mg/kg body weight) caused reduction in hepatic glutathione content and the activities of hepatic anti-oxidant enzymes and phase-II metabolizing enzymes with an enhancement of xanthine oxidase activity, lipid peroxidation and hydrogen peroxide content. 2-AAF treatment also induced serum oxaloacetate and pyruvate transaminase, lactate dehydrogenase and gamma-glutamyl transpeptidase. Treatment of rats orally with tannic acid (125 and 250 mg/kg body weight) resulted in significant recovery of hepatic glutathione content, antioxidant and phase-II metabolizing enzymes. Also, significant decreases in lipid peroxidation, xanthine oxidase, hydrogen peroxide generation and liver damage marker enzymes were observed. The antiproliferative efficacy of the tannic acid was also evaluated. The promotion parameters induced (ornithine decarboxylase activity and DNA synthesis) by 2-AAF administration in the diet with partial hepatectomy (PH) were also significantly suppressed, dose dependently, by tannic acid. Hence, we propose that tannic acid might suppress the promotion stage via inhibition of oxidative stress and polyamine biosynthetic pathway.
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PMID:Preventive effect of tannic acid on 2-acetylaminofluorene induced antioxidant level, tumor promotion and hepatotoxicity: a chemopreventive study. 1668 99

The antioxidative effects of pumpkin seed protein isolate (Cucurbita pepo) were investigated in vitro. The isolate exhibited about 80% radical scavenging activity, chelating activity of approximately 64% on Fe2+ ions and an inhibition of approximately 10% of xanthine oxidase. Subsequently the effects of the isolate on the plasma activity levels of alanine transaminase and aspartate transaminase against acetaminophen induced acute liver injury in low-protein fed male Sprague-Dawley rats were ascertained. The rats were maintained on a low-protein diet for 5 days and divided into three subgroups. Two subgroups were injected with acetaminophen and the other with an equivalent amount of polyethylene glycol 400. Two hours after intoxication one of the two subgroups was administered with the protein isolate. Rats from the different subgroups were killed at 24, 48 and 72 h after treatment. After 5 days on the low-protein diet the activity levels of the enzymes were significantly higher than their counterparts on a normal balanced diet. The administration of protein isolate after acetaminophen intoxication resulted in significantly reduced activity levels. It is concluded that the protein isolate has promising antioxidative properties. Furthermore, the isolate administration was effective in alleviating the detrimental effects associated with protein malnutrition and acetaminophen intoxication.
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PMID:In Vitro antioxidative activity of pumpkin seed (Cucurbita pepo) protein isolate and its In Vivo effect on alanine transaminase and aspartate transaminase in acetaminophen-induced liver injury in low protein fed rats. 1680 84

It is well known that formaldehyde (FA) and reactive oxygen species (ROS) are cytotoxic and potentially carcinogenic. Although the individual effects of these reactants on cells have been investigated, the cytotoxicity exerted by the coexistence of FA and ROS is poorly understood. The present study was carried out to evaluate oxidant/antioxidant status and biochemical changes occurring after chronic formaldehyde toxicity in liver tissue and plasma of rats and protective effect of vitamin E (vit E) against oxidative damage. Eighteen rats were divided into three groups: (1) control rats, (2) rats treated with FA (FAt), and (3) rats treated with FA plus vit E (FAt + vit E) groups. After the treatment, the animals were sacrificed and liver tissues were removed for biochemical investigations. As a result, FA treatment significantly increased the levels of tissue malondialdehyde (MDA), protein carbonyl (PC), nitric oxide (NO) and the activity of xanthine oxidase enzyme (XO). On the other hand, FA exposure led to decrease in superoxide dismutase (SOD) and catalase (CAT) activities in liver tissues compared to control. FA caused significant decreases in total protein (TP) and albumin (ALB) whereas increases in aspartate transaminase (AST), alanine aminotransferase (AST), alkaline phosphatase (ALP) and interleukine-2 (IL-2) levels in plasma. Vit E treatment abolished these changes at a level similar to the control group. It was concluded that vit E treatment might be beneficial in preventing FA-induced liver tissue damage, and therefore have potential for clinical use.
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PMID:Vitamin E protects against oxidative damage caused by formaldehyde in the liver and plasma of rats. 1693 16

Elevated plasma levels of xanthine oxidase and liver function parameters have been associated with inflammatory events in several human diseases. While xanthine oxidase provides in vitro protection against malaria, its pathophysiological functions in vivo and interactions with liver function parameters remain unclear. This study examined the interactions and plasma levels of xanthine oxidase (XO) and uric acid (UA), catalase (CAT) and liver function parameters GOT, GPT and bilirubin in asymptomatic (n=20), uncomplicated (n=32), and severe (n=18) falciparum malaria children aged 3-13 years. Compared to age-matched control (n=16), significant (p<0.05) elevation in xanthine oxidase by 100-550%, uric acid by 15.4-153.8%, GOT and GPT by 22.1-102.2%, and total bilirubin by 2.3-86% according to parasitaemia (geometric mean parasite density (GMPD)=850-87100 parasites/microL) was observed in the malarial children. Further comparison with control revealed higher CAT level (16.2+/-0.5 vs 14.6+/-0.4 U/L; p<0.05) lacking significant (p>0.05) correlation with XO, but lower CAT level (13.4-5.4 U/L) with improved correlations (r=-0.53 to -0.91; p<0.05) with XO among the asymptomatic and symptomatic malaria children studied. 75% of control, 45% of asymptomatic, 21.9% of uncomplicated, and none of severe malaria children had Hb level>11.0 g/dL. Multivariate analyses further revealed significant (p<0.05) correlations between liver function parameters and xanthine oxidase (r=0.57-0.64) only in the severe malaria group. We conclude that elevated levels of XO and liver enzymes are biochemical features of Plasmodium falciparum parasitaemia in Nigerian children, with both parameters interacting differently to modulate the catalase response in asymptomatic and symptomatic falciparum malaria.
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PMID:Levels and interactions of plasma xanthine oxidase, catalase and liver function parameters in Nigerian children with Plasmodium falciparum infection. 1720 84

This study investigated the effect of sesamol (3,4-methylenedioxyphenol) on systemic oxidative stress and hepatic function in acutely iron-intoxicated mice. Sesamol reduced the levels of lipid peroxidation, hydroxyl radical, iron production and superoxide anion generation, and xanthine oxidase activity in iron-intoxicated mice. In addition, sesamol decreased the serum levels of aspartate aminotransferase and alanine aminotransferase, and ameliorated iron-intoxication-induced histological changes in the liver. In summary, sesamol might attenuate systemic oxidative stress by reducing xanthine oxidase and improving hepatic function in iron-intoxicated mice.
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PMID:The effect of sesamol on systemic oxidative stress and hepatic dysfunction in acutely iron-intoxicated mice. 1758 87

We examined how oxidative stress and cell damage develop in the liver of rats subjected to water-immersion stress (WIRS). In rats subjected to WIRS for 1.5, 3 or 6 h, serum alanine aminotransferase and aspartate aminotransferase activities increased time-dependently. In the liver tissue, vacuolization and apoptosis occurred at 1.5 h of WIRS and vacuolization further developed without further appearance of apoptosis at 3 h or 6 h. Serum lipid peroxide (LPO) and NOx (nitrite/nitrate) concentrations increased at 3 h of WIRS and these increases were enhanced at 6 h. In liver tissue, increases in LPO and NOx concentrations and myeloperoxidase activity and decreases in ascorbic acid and reduced glutathione concentrations and superoxide dismutase activity occurred at 3 h of WIRS and these changes were enhanced at 6 h, although vitamin E concentration and xanthine oxidase activity were unchanged. These results indicate that oxidative stress in the liver of rats with WIRS develops after the appearance of cell damage in the tissue, and suggests that oxidative stress is caused through disruption of the antioxidant defense system and increases in NO generation and neutrophil infiltration in the liver, which may contribute to the progression of cell damage in the tissue.
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PMID:Development of oxidative stress and cell damage in the liver of rats with water-immersion restraint stress. 1762 21

This study was carried out to investigate the anti-oxidative and hepatoprotective effects of glycoprotein isolated from Zanthoxylum piperitum DC fruit (ZPDC glycoprotein). ZPDC glycoprotein showed a single band with molecular weight of 24kDa on the 18% sodium dodecyl sulfate-polyacrylamide gel and consists of a carbohydrate component (18%) and a protein component (82%). We found that ZPDC glycoprotein has a strong scavenging activity against DPPH, superoxide anion, and hydroxyl radicals without any pro-oxidant activity in the cell-free system. In hepatocyte cell lines (Chang liver and BNL CL.2 cells), the results showed that ZPDC glycoprotein has an inhibitory effect on hypoxanthine/xanthine oxidase- or glucose/glucose oxidase-induced cytotoxicity in a dose-dependent manner. In addition, administration of ZPDC glycoprotein (20mg/kg) lowers the levels of lactate dehydrogenase, alanine transaminase, and thiobarbituric acid reactive substances, whereas increases that of nitric oxide, accompanying the normalizing effects on the activity of hepatic anti-oxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase) in mouse model of carbon tetrachloride-stimulated acute liver injury. On the whole the results suggest that ZPDC glycoprotein can be a potent hepatoprotective agent as a natural anti-oxidant.
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PMID:Glycoprotein of Zanthoxylum piperitum DC has a hepatoprotective effect via anti-oxidative character in vivo and in vitro. 1802 43

Increased oxidative stress and associated high levels of free radical generation have been described to occur during the pathogeneses of various diseases in animal models. In the present work, we investigated the protective effects of the phenethyl ester of caffeic acid (CAPE), an active component of honeybee propolis, on tert-butyl hydroperoxide (t-BHP)-induced hepatotoxicity in a cultured HepG2 cell line and in rat liver. CAPE was found to significantly reduce t-BHP-induced oxidative injury in HepG2 cells, as determined by cell cytotoxicity, and lipid peroxidation and reactive oxygen species (ROS) levels in a dose-dependent manner. Furthermore, CAPE protected HepG2 cells against t-BHP-induced oxidative DNA damage, as determined by the Comet assay. Consistently, CAPE reduced hydroxyl radical-induced 2-deoxy-d-ribose degradation by ferric ion-nitrilotriacetic acid and H2O2, and also removed the superoxide anion generated by a xanthine/xanthine oxidase system. Our in vivo study showed that pretreatment with CAPE prior to the administration of t-BHP significantly and dose-dependently prevented increases in the serum levels of hepatic enzyme markers (alanine aminotransferase and aspartate aminotransferase) and reduced lipid peroxidation in rat liver. Moreover, histopathological evaluation of livers consistently revealed that CAPE reduced liver lesion induction by t-BHP. Taken together, these results suggest that the protective effects of CAPE against t-BHP-induced hepatotoxicity may, at least in part, be due to its ability to scavenge ROS and protect DNA from oxidative stress-induced damage.
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PMID:Protective effect of caffeic acid phenethyl ester on tert-butyl hydroperoxide-induced oxidative hepatotoxicity and DNA damage. 1848 57


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