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 protective effects of water extract of Du-Zhong (Eucommia ulmoides Oliv.) leaves (WEDZ) and its active compound (protocatechuic acid; PCA) on liver damage were evaluated by carbon tetrachloride (CCl4)-induced chronic hepatotoxicity in rats. Wistar rats were orally treated with WEDZ (0.1, 0.5, and 1.0 g/kg bw) or PCA (0.1 g/kg bw) with administration of CCl4 (0.5 ml/rat, 20% CCl4 in olive oil) for 28 consecutive days. It showed that CCl4-treated rats increased the relative organ weights of liver and kidney. CCl4-induced rats liver damage and significantly (p<0.05) increased the GOT, GPT, LDH and ALP levels in serum as compared with the control group. Treatment with WEDZ or PCA could decrease the GOT, GPT, LDH and ALP levels in serum when compared with CCl4-treated group. CCl4-treated rats also significantly (p<0.05) decreased the GSH content in liver and trolox equivalent antioxidant capacity (TEAC) in serum whereas increased (p<0.05) MDA content in liver as compared with the control group. Treatment with WEDZ or PCA also significantly (p<0.05) increased the GSH content and significantly (p<0.05) decreased the MDA content in liver. Administration of WEDZ or PCA could increase the activities of GPx, GRd and GST in liver. Liver histopathology showed that WEDZ or PCA reduced the incidence of liver lesions including hepatic cells cloudy swelling, lymphocytes infiltration, cytoplasmic vacuolization, hepatic necrosis and fibrous connective tissue proliferated induced by CCl4 in rats. The data suggest that oral administration with WEDZ for 28 consecutive days significantly decrease the intensity of hepatic damage induced by CCl4 in rats.
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PMID:Du-Zhong (Eucommia ulmoides Oliv.) leaves inhibits CCl4-induced hepatic damage in rats. 1670 2

Mice primed by feeding griseofulvin or diethyl 1,4-dihydro 1,4,6-trimethyl 3,5-pyridine decarboxylate for 5 months followed by drug withdrawal for 1 month (drug-primed mice) were given thioacetamide intraperitoneally, and the livers were subsequently studied at intervals up to 7 days. The hepatocellular proliferative response was measured by immunostaining for proliferative cell nuclear antigen. Necrosis was followed by measuring ALT. Mallory bodies were identified by immunoperoxidase stains for ubiquitin and cytokeratin. Preneoplastic foci were localized using immunofluorescence stain for glutathione S-transferase (GST mu) and histochemical stain for gamma glutamyl transpeptidase (GGT). The results showed that the preneoplastic foci selectively proliferated and expanded and formed nodules as indicated by quantitation of nuclei stained positive for proliferating cell nuclear antigen after thioacetamide treatment. Data support the hypothesis that the preneoplastic foci consisted of clones of hepatocytes which preferentially express GST mu, GGT and Mallory bodies. These preneoplastic cells selectively proliferate in response to the promoter effects of necrosis-induced liver cell regeneration ("chemical partial hepatectomy").
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PMID:Preneoplastic liver cell foci expansion induced by thioacetamide toxicity in drug-primed mice. 1672 98

Hepatic damage associated with chronic hepatitis B (CHB) relies on measurement of serum transaminases and asssessment of hepatic histology. We determined if serum hepatic function tests, including alpha-glutathione-S-transferase ((GST), were of value in monitoring or predicting the effect of lamivudine therapy for CHB. Thirty-nine patients received orally 100 mg of lamivudine daily for 48 weeks. Blood samples were obtained at baseline and at 24 and 48 weeks. At the end of the treatment period the patients were then divided into four groups according to the pattern of HBs and HBe antigens. At baseline and at 24 weeks ALT, AST, and (GST had lower values in the complete response compared to the complete failure groups. Using ROC analysis, only ALT at 24 weeks (area under the curve = 0.803) had significant diagnostic ability in detecting responders. These results reaffirm the value of measuring serum ALT as an indicator of treatment response and provide information on the potential use of (GST as an additional prognostic biomarker in this patient group.
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PMID:Evaluation of alpha-glutathione-S-transferase as a biomarker of lamivudine therapy for chronic hepatitis B. 1698 2

The effects of polysaccharide peptide (PSP), an immunomodulator isolated from Coriolus versicolor COV-1, on glutathione (GSH) and GSH-related enzymes was investigated in C57 mouse. Administration of PSP (1-4 micromole/kg, i.p.) produced a transient, dose-dependent depletion (10-37%) of hepatic GSH, with no effect on serum glutamic-pyruvic transaminase (SGPT) activity. Blood GSH was depleted (6-25%) at 3 h, followed by a rebound increase above the control GSH level (20%) at 18 h. The GSSG/GSH ratio, a measure of oxidative stress, was increased 3 h after PSP treatment but returned to normal levels at 24 h. Sub-chronic treatment of PSP (1-4 micromole/kg/day, i.p.) for seven days did not produce any significant changes in hepatic GSH levels and the GSSG/GSH ratio when measured 24 h after the final dose of PSP. PSP had little effect on glutathione transferase (GST), glutathione reductase (GSSG reductase) and glutathione peroxidase (GPX) activities in the liver. However, a dose-dependent increase in blood GPX activity (30-48%) was observed at 3h, which coincided with the increase in the GSSG/GSH ratio. The increase in blood GPX activity may be a responsive measure to deal with the transient oxidative stress induced by PSP treatment. The results showed that PSP only caused a transient perturbation on hepatic glutathione without affecting the GSH-related enzymes such as GST, GSSG reductase and GPX. The observed changes in blood GSH simply reflected the intra-organ translocation of glutathione, as the glutathione-related enzymes were not significantly affected by PSP treatment.
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PMID:Effects of polysaccharide peptides from COV-1 strain of Coriolus versicolor on glutathione and glutathione-related enzymes in the mouse. 1724 May 8

Hepatitis C Virus (HCV) infection is a disease characterized by a silent evolution, a wide fluctuation of transaminase activities, and the potential presence of significant histological lesions in patients with normal concentrations of transaminases. Alpha-Glutathione S-transferase (alpha-GST) is a class of enzymes responsible for cellular detoxifying processes. Its wide hepatic distribution, high cytosolic concentration, and short in vivo plasma half-life of this enzyme are properties, which may make monitoring this enzyme more clinically useful than conventional biochemical liver function tests as a marker of hepatocellular damage. This work was designed to study whether determining alpha-GST compared to other biochemical parameters might improve the assessment of patients with HCV infection, and to determine whether the increase in alpha-GST concentrations could reflect HCV viraemia. A total of 68 HCV infected patients along with 20 anti-HCV negative healthy subjects were enrolled in this study. HCV infected patients were tested for the presence of HCV RNA in their sera by polymerase chain reaction and evaluated with conventional liver biochemistry (ALT, AST and gamma-GT). Alpha-GST concentrations were determined in all cases and control subjects included in the study using an enzyme immunoassay. HCV viraemia was found in 36/68( 52.9%) seropositive patients. Alpha-GST levels were markedly elevated in HCV infected subjects compared to healthy controls (P < 0.001). Alpha-GST values were significantly higher than the cut off value in the 36 HCV viraemic patients compared to 81.3% of the HCV RNA-negative subjects (P < 0.05). The estimated alpha-GST concentrations were significantly above the cut off value in 91.2% of HCV infected subjects compared to 4.4% for ALT, 17.6% for AST and 41.2 % for gamma-GT (P < 0.001). In conclusion, measurement of alpha-GST levels in HCV infected patients could reflect liver injury more than biochemical markers. Therefore, it is possible that in combination with the other traditionally used liver markers; alpha-GST determination could provide another parameter, which may play a complimentary role in the assessment of hepatocellular damage caused by HCV.
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PMID:Diagnostic value of alpha-glutathione S-transferase as a sensitive marker of increased risk for hepatocellular damage in hepatitis C virus (HCV) infection: relation to HCV viraemia. 1726 14

Our aim was to study the protective effect of quercitin on liver cirrhosis induced by carbon tetrachloride (CCl(4)) in rats and its relationship with liver morphology. Thirty male Wistar rats weighing 200-250 g were randomly divided into three groups: control, CCl(4), and CCl(4)+ quercetin. Rats in the experimental groups were given CCl(4) (0.5 ml/kg i.p.), diluted 1:6 in vegetable oil (5 mmol/kg body wt), at 10:00 p.m. every 4 days for 17 weeks. Quercetin (500 microl/kg i.p.; 150 micromol/kg body wt) or vehicle was administered at 6:00 p.m. for the last 3 weeks of the study. Control group rats were given only olive oil for the same period. At the end of the 17 weeks, all rats were sacrificed. Blood samples were taken for determination of serum indicators (ALT, AST, total bilirubin, conjugated bilirubin, factor V) and the livers were dissected out and divided into two parts: one was homogenized and the supernatant was used for measurement of superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) activities, as well as lipid peroxidation. The other part was used for the histopathological study. CCl(4) caused a marked rise in serum levels of ALT, AST, total bilirubin, and conjugated bilirubin, as well as a decrease in factor V (P<0.05). Lipid peroxidation levels were significantly increased, whereas GSH, SOD, catalase, GPx, and GST levels were decreased in the liver of CCl(4)-treated rats. Quercetin (50 mg/kg/day) successfully attenuated these effects of CCl(4). We conclude that quercetin has beneficial effects on liver fibrosis in rats by enhancing antioxidant enzyme activity and decreasing the pro-oxidant effect.
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PMID:Quercetin prevents oxidative stress in cirrhotic rats. 1743 69

Wild Panax ginseng C.A. Meyer (WG) is a well-known medicinal herb. In this study, the protective effects of a water extract from the root of WG on benzo[alpha]pyrene (BP)-induced hepatotoxicity and the mechanism of these effects were investigated for the first time. The effects of WG on liver toxicities induced by BP were assessed by blood biochemical and histopathological analyses. BP caused severe liver injury in rats, as indicated by elevated plasma ALT, AST and LPO levels. Pretreatment with WG for 4 weeks completely abrogated increases in the ALT, AST and LPO levels when challenged with BP. Reductions in GSH content and GST activity by BP were reversed by WG. These protective effects of WG against BP-induced toxicity were consistent with the results of histopathological examinations. We next examined the effects of WG on the gene expression of the enzymes that metabolize BP in H4IIE cells. CYP1A1 mRNA and protein expression were increased by BP. WG moderately inhibited BP-induced CYP1A1 gene expression. Moreover, GSTA2, GSTA3 and GSTM2 gene expressions were significantly increased by WG through the Nrf2/antioxidant responsive element pathway for enzyme induction. In summary, WG is efficacious in protecting against BP-induced hepatotoxicity as results of metabolic regulations through both the inhibition of metabolic enzyme activation and the enhancement of electrophilic detoxification, implying that WG should be considered a potential chemopreventive agent.
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PMID:The potent protective effect of wild ginseng (Panax ginseng C.A. Meyer) against benzo[alpha]pyrene-induced toxicity through metabolic regulation of CYP1A1 and GSTs. 1759 Feb 95

Penicillin and other antibiotics are routinely incorporated in insect culture media. Although culturing insects in the presence of antibiotics is a decades-old practice, antibiotics can exert deleterious influences on insects. In this article, we test the hypothesis that one of the effects of dietary penicillin is to increase oxidative stress on insects. The effects of penicillin on midgut concentrations of the oxidative stress indicator malondialdehyde (MDA) and on midgut antioxidant enzyme (superoxide dismutase [SOD], catalase [CAT], glutathione S-transferase [GST], and glutathione peroxidase [GPx]) and transaminases (alanine aminotransferase and aspartate aminotransferase) activities in greater wax moth, Galleria mellonella (L.), were investigated. The insects were reared from first instars on artificial diets containing 0.001, 0.01, 0.1, or 1.0 g penicillin per 100 g of diets. MDA content was significantly increased in the midgut tissues of each larval instar reared in the presence of high penicillin concentrations. Activities of antioxidant and transaminase enzymes did not show a consistent pattern with respect to penicillin concentrations in diet or age of larvae. Despite the increased penicillin-induced oxidative stress in gut tissue, antioxidant and transaminase enzymes did not correlate with oxidative stress level or between each other in larvae of other age stages except for the seventh instar. We found a significant negative correlation of MDA content with SOD and GST activities in seventh instars. SOD activity was also negatively correlated with CAT activity in seventh instars. These results suggest that exposure to dietary penicillin resulted in impaired enzymatic antioxidant defense capacity and metabolic functions in wax moth larval midgut tissues and that the resulting oxidative stress impacts midgut digestive physiology.
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PMID:Penicillin-induced oxidative stress: effects on antioxidative response of midgut tissues in instars of Galleria mellonella. 1797 30

Increased oxidative stress and antioxidant deficit have been suggested to play a major role in isoproterenol-induced myocardial infarction. The present study was designed to evaluate the effect of alpha-mangostin on the antioxidant defense system and lipid peroxidation against isoproterenol-induced myocardial infarction in rats. Induction of rats with ISO (150 mg/kg body weight, ip) for 2 days resulted in a marked elevation in lipid peroxidation, serum marker enzymes (LDH, CPK, GOT, and GPT) and a significant decrease in the activities of endogenous antioxidants (SOD, CAT, GPx, GST, and GSH). Pre-treatment with alpha-mangostin (200 mg/kg of body weight per day) orally for 6 days prior to the ISO administration and 2 days along with ISO administration significantly attenuated these changes when compared to the individual treatment groups. These findings indicate the protective effect of alpha-mangostin on lipid peroxidation and antioxidant tissue defense system during ISO-induced myocardial infarction in rats.
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PMID:Cardioprotective effect of alpha-mangostin, a xanthone derivative from mangosteen on tissue defense system against isoproterenol-induced myocardial infarction in rats. 1799 76

Solanum nigrum L. (SN) is an herbal plant that has been used as hepatoprotective and anti-inflammation agent in Chinese medicine. In this study, the protective effects of water extract of SN (SNE) against liver damage were evaluated in carbon tetrachloride (CCl4)-induced chronic hepatotoxicity in rats. Sprague-Dawley (SD) rats were orally fed with SNE (0.2, 0.5, and 1.0 g kg(-1) bw) along with administration of CCl4 (20% CCl4/corn oil; 0.5 mL kg(-1) bw) for 6 weeks. The results showed that the treatment of SNE significantly lowered the CCl4-induced serum levels of hepatic enzyme markers (GOT, GPT, ALP, and total bilirubin), superoxide and hydroxyl radical. The hepatic content of GSH, and activities and expressions of SOD, GST Al, and GST Mu that were reduced by CCl4 were brought back to control levels by the supplement of SNE. Liver histopathology showed that SNE reduced the incidence of liver lesions including hepatic cells cloudy swelling, lymphocytes infiltration, hepatic necrosis, and fibrous connective tissue proliferation induced by CCl4 in rats. Therefore, the results of this study suggest that SNE could protect liver against the CCl4-induced oxidative damage in rats, and this hepatoprotective effect might be contributed to its modulation on detoxification enzymes and its antioxidant and free radical scavenger effects.
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PMID:Hepatoprotective effects of Solanum nigrum Linn extract against CCl(4)-induced oxidative damage in rats. 1804 81


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