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)

In the present study, an investigation was undertaken to assess the efficacy on serum enzymes of colloidal bismuth subcitrate (CBS). CBS was administered with injections to male rats in 100-, 200-, 400-, 500-, and 1000-microg/L doses of bismuth. Rats were anesthetized at different intervals (24, 48, and 72 h) after CBS injections. The levels of serum enzymes were determined. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and creatine kinase (CK) levels significantly increased after all CBS treatments without dependence on time. All doses of bismuth significantly affected the lactate dehydrogenase (LDH) in serum after 72 h. The lowest doses were the most toxic on ALT and LDH. These data suggest that treatment with CBS can provide evidence for a possible marker of liver toxicity although there is no evidence of liver accumulation of bismuth in the present study.
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PMID:Biochemical response to colloidal bismuth subcitrate: dose-time effect. 1603 60

Stannous chloride (SnCl2) is widely used in daily human life to conserve soft drinks, in food manufacturing and biocidal preparations. It had genotoxicity, immunotoxicity, neurotoxicity and oxidative stress. Therefore, the present experiment was carried out to determine the effectiveness of l-ascorbic acid (AA) in alleviating the toxicity of SnCl2 on some enzyme activities and oxidative damage in male New Zealand white rabbits. Six rabbits per group were assigned to 1 of 4 treatment groups: 0 mg AA and 0 mg SnCl2/kg BW (control); 40 mg AA/kg BW; 20 mg SnCl2/kg BW (1/500 LD50); 20 mg SnCl2 plus 40 mg AA/kg BW. Rabbits were orally administered the respective doses every other day for 12 weeks. Liver and kidney specimens were processed for histopathologic studies. Results obtained showed that SnCl2 significantly (P < 0.05) induced free radicals in rabbit liver, testes, kidney, lung, brain and heart. While, the activity of glutathione S-transferase (GST) and the level of sulfhydryl groups (SH-group) were decreased (P < 0.05) in all tested organs except brain and heart. Aspartate aminotransferase (AST) activity was increased (P < 0.05) in liver and decreased in testes, but alanine aminotransferase (ALT) did not change. The activities of alkaline phosphatase (AlP) and acid phosphatase (AcP) were decreased (P < 0.05) in liver, testes, kidney and lung. Also, the activity of acetylcholinesterase (AChE) was significantly decreased in brain and plasma of rabbits treated with SnCl2 compared to control group. Histopathologic studies showed marked changes in hepatocytes as well as proliferation of duct epithelium, dilatation and congestion of blood vessels as well as mononuclear inflammatory infiltrate. The kidney were also severely affected by SnCl2 the Bowman's space was increased, with infiltration of renal parenchyma by mononuclear inflammatory infiltrate and changes in cells lining convoluted tubule. Ascorbic acid alone significantly decreased the levels of free radicals, and increased the activity of GST and the levels of SH groups in tested organs except brain and heart. While, the rest of the tested parameters were not affected. Results showed that AA alleviated the harmful effects of SnCl2. This was proved histopathologically by the great improvement in liver and kidney histology where hepatocytes retained normal architecture with mild dilatation and congestion of blood vessels. Bowman's space of kidney was almost normal, with normal lining of proximal and distal convoluted tubules. In conclusion AA could be effective in the protection against stannous chloride toxicity.
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PMID:Stannous chloride induces alterations in enzyme activities, lipid peroxidation and histopathology in male rabbit: antioxidant role of vitamin C. 1605 10

The patient's position during laparoscopic surgery can have a clinically relevant effect on lower limb and splanchnic circulation; this factor has not yet been investigated with respect to oxidative stress markers. In order to assess this effect, a prospective clinical trial was designed wherein 2 groups of patients were studied. In group A, 15 patients underwent upper abdominal nonhepatobiliary operations (13 modified Nissen fundoplications and 2 Taylor vagotomies) in the head-up position. In group B, 15 patients underwent lower abdominal operations (10 laparoscopic colectomies and 5 inguinal hernia repairs) in the head-down position. The pneumoperitoneum was maintained at 14 mm Hg in all cases. Plasma concentrations of thiobarbituric-acid reactive substances (TBARS), a marker of lipid peroxidation, plasma total antioxidant status (TAS), and serum uric acid concentrations were measured preoperatively, 5 minutes after deflation of the pneumoperitoneum, and 24 hours postoperatively. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) serum activities were measured preoperatively and 24 hours postoperatively. In group A, there was a significant increase in TBARS levels (p<0.005) immediately after deflation of the pneumoperitoneum and a significant decrease in TAS and uric acid levels (p<0.005) in the first postoperative day. There was also a significant postoperative elevation in both ALT and AST activities (p<0.001). In group B, no significant increase was found in postoperative TBARS or transaminase levels. TAS and uric acid levels decreased significantly in the first postoperative day (p<0.05) and (p<0.005, respectively). In conclusion, these results show that a combination of pneumoperitoneum and the head-up position causes significant increase in lipid peroxidation, decrease in plasma TAS, and increase in transaminases. The mechanism responsible for these events could be the low-flow ischemia-reperfusion syndrome induced by the pneumoperitoneum and aggravated by the head-up position.
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PMID:Alterations in plasma oxidative stress markers after laparoscopic operations of the upper and lower abdomen. 1607 30

The impact of 3 different reperfusion sequences following orthotopic liver transplantation (OLT) in pigs were evaluated. The reperfusion technique commonly performed is primary portal in order to shorten warm ischemic times (WITs). Experimental and clinical data, usually comparing 2 out of 3 possible reperfusion sequences, provide controversial results. OLT was performed in 24 pigs randomized into 3 groups: primary arterial (A), simultaneous (SIM), and primary portal (P) reperfusion. Hemodynamics were continuously monitored and reperfusion injury and primary graft function were assessed by standard serum parameters, histopathological findings, immunohistochemistry for heme oxygenase 1 (HO-1), and heat shock protein 70 (HSP 70). Aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and gamma-glutamyl transpeptidase (gammaGT) following reperfusion were significantly increased for group A when compared to groups SIM and P. Hemodynamics showed significant differences after reperfusion compared to physiological data; differences in group comparisons were not significant. The bile production/100 g liver/hr was significantly higher for group SIM (1.15 mL) compared to group P (0.66 mL) and group A (0.62 mL). Histology and immunohistochemistry significantly correlated with functional results and outcome. Histological score was best for group SIM and worst for group A. HSP 70, being visualized mainly in the hepatocytes, showed higher expression for groups SIM and P. Inversely, HO-1, found in perisinusoidal cells, showed highest expression after primary arterial reperfusion. In conclusion, although associated with a 10-minute longer warm ischemic time, simultaneous reperfusion causes the least reperfusion injury with superior primary transplant function. Primary arterial reperfusion showed the worst overall outcome and highest degree of HO-1 expression.
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PMID:Sequence of reperfusion influences ischemia/reperfusion injury and primary graft function following porcine liver transplantation. 1618 69

In view of a role of oxidative stress in epilepsy and the evidence for the involvement of peroxidative injury in sodium valproate (SVP)-induced adverse effects on liver and kidneys, we investigated whether the combination of SVP with N-acetylcysteine (NAC), an antioxidant, may help us to achieve maximal efficacy in terms of seizure control, with minimal toxicity on liver and kidneys. Pentylenetetrazole (PTZ)-induced seizures were used to evaluate the anticonvulsant effect of drugs. Biochemical estimations included the determination of oxidative stress markers like thiobarbituric acid-reactive substances in brain tissue and glutathione (GSH) levels in liver and kidney tissues. Aspartate aminotransferase and alanine aminotransferase concentrations in the serum were also determined to assess liver function. In our study, NAC exhibited a nondose-dependent anticonvulsant effect. The concurrent administration of NAC with SVP significantly prolonged the latency to jerks, myoclonus and clonic generalized seizures. No significant oxidative stress was evident in brain tissue following PTZ-induced seizures, though an elevation of serum transaminase enzymes was seen. SVP at the dose studied did not produce any significant oxidative stress on the liver and kidneys, while treatment with NAC elevated liver and kidney GSH levels. The concurrent administration of NAC with SVP had beneficial effects on liver and kidney cells.
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PMID:Modulation of pentylenetetrazole-induced seizures and oxidative stress parameters by sodium valproate in the absence and presence of N-acetylcysteine. 1667 59

Cholestasis-induced liver injury during bile duct obstruction causes an inflammatory response and this inflammatory process may be an important source of tissue injury. We hypothesized that NF-kappaB inhibition would decrease liver injury in a rat model of extrahepatic biliary obstruction. A total of 40 female rats of Sprague-Dawley strain were allocated to four groups. First group was sham operated control. The second group underwent common bile duct ligation (BDL) and was monitored for 10 days. Third group of rats underwent BDL and received pyrrolidine dithiocarbomate (PDTC) at a dose of 100 mg/kg/day intraperitoneally. Fourth group underwent BDL and received sulfasalazine at a dose of 100 mg/kg b.w. Both inhibitors were administered once a day throughout last 7 days of the experimental period. Rats were terminated 10 days after sham operation or BDL. Aspartate aminotransferase, alanine aminotransferase, gamma-glutamil transpeptidase, and tumor necrosis factor-alpha levels were elevated in the BDL group as compared to the control group, while this increase was significantly decreased by treatment with PDTC and sulfasalazine (P < 0.05). Hepatic GSH, SOD and catalase levels were significantly depressed by BDL, but were elevated back to control levels in NF-kappaB inhibitor-treated BDL groups. Increases in tissue free radical and MDA levels and MPO activity due to BDL were reduced back to control levels by NF-kappaB inhibitor treatment (P < 0.05). Similarly histological damage in the BDL rats was reduced by treatments. These results indicate that inhibitors of NF-kappaB activity such as PDTB and sulfasalazine exert a therapeutic effect on cholestatic liver injury in rats with BDL through anti-inflammatory and antioxidant actions.
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PMID:The NF-kappaB inhibitors attenuate hepatic injury in bile duct ligated rats. 1683 Jan 61

We have recently described the presence of occult hepatitis C virus (HCV) infection (HCV-RNA in liver in the absence of anti-HCV and serum HCV-RNA) in patients with persistently abnormal liver function tests of unknown aetiology. The aim of this study was to compare the characteristics of patients with occult HCV infection vs those of patients with chronic hepatitis C. We compared clinical features of 68 patients with occult HCV infection and 69 untreated chronic HCV patients (anti-HCV and serum HCV-RNA positive), matched for age, gender, duration of abnormal liver function tests and body mass index. Aspartate aminotransferase and alanine aminotransferase were higher (P < 0.001) in chronic HCV, but cholesterol and triglycerides were significantly higher in patients with occult HCV infection (P < 0.001 and P = 0.002). Chronic HCV patients had higher gamma-globulin (P = 0.005), alpha-foetoprotein (P < 0.001) and iron (P < 0.001) levels. Percentage of patients with necroinflammatory activity and fibrosis was higher (P < 0.001) in chronic HCV than in occult HCV infection. Mean percentage of infected hepatocytes was higher (P = 0.001) in chronic HCV (10.1%) than in occult HCV infection (5.3%). This occult HCV infection is a milder disease than chronic HCV, and this could be related to the significantly lower number of infected hepatocytes observed in occult HCV.
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PMID:Comparative study between occult hepatitis C virus infection and chronic hepatitis C. 1721 42

Lead (Pb) increases lipopolysaccharide (LPS)-induced tumor necrosis factor alpha, which causes liver damage. In this study, we investigated the effect of sesame oil on Pb-plus-LPS (Pb + LPS)-induced acute liver damage in mice. Mice were given sesame oil (8 mL/kg orally) just after Pb acetate (10 mmol/kg i.p.) plus LPS (5 mg/kg i.p.). Aspartate aminotransferase, alanine aminotransferase, tumor necrosis factor-alpha, interleukin-1beta, nitric oxide, and inducible nitric oxide synthase levels were examined. Sesame oil significantly decreased serum aspartate aminotransferase and alanine aminotransferase levels in Pb + LPS-stimulated mice. Sesame oil reduced Pb + LPS-induced tumor necrosis factor-alpha, interleukin-1beta, and nitric oxide production in serum and liver tissue. Furthermore, sesame oil decreased inducible nitric oxide synthase expression in leukocytes and liver tissue in Pb + LPS-treated mice. We hypothesize that the inhibition of proinflammatory cytokines and nitric oxide might be involved in sesame oil-associated protection against Pb + LPS-induced acute hepatic injury in mice.
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PMID:Sesame oil protects against lead-plus-lipopolysaccharide-induced acute hepatic injury. 1730 16

We sought to evaluate the effects of pentoxifylline (PTX) on steatohepatitis in a novel experimental nonalcoholic steatohepatitis (NASH) model induced by a high-fat diet (HFD). Thirty-three male Sprague-Dawley rats were randomly divided into 3 groups. The first group received only standard rat diet (control group); groups 2 (placebo group) and 3 were given HFD, ad libitum. After week 4, 0.5 mL of physiologic serum was injected subcutaneously to the placebo group and 50 mg/kg/d PTX was given intraperitoneally to the third group (group PTX). After 6 weeks all rats were humanely killed. Serum biochemistry, tumor necrosis factor-alpha (TNF-alpha), plasma, and liver tissue malondialdehyde (MDA) were analyzed. Histopathologically, steatosis, ballooning degeneration, inflammation, and fibrosis were determined. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, plasma and liver tissue MDA, and plasma TNF-alpha levels were significantly higher in placebo group than in the control group. Tumor growth factor-beta levels, however, were comparable in the placebo and control groups. On histopathologic examination, steatosis, inflammatory cells per square millimeter, and ballooning degeneration were significantly higher in the placebo group than in the control group. No fibrosis or Mallory bodies were found in the placebo group. AST, ALT, plasma and liver tissue MDA, and plasma TNF-alpha levels were significantly lower in PTX group compared to the placebo group. Histopathologically, steatosis, mean number of inflammatory cells/mm(2) and ballooning degeneration in PTX group were also significantly lower than in the placebo group. In conclusion, PTX strikingly ameliorates steatohepatitis in this novel NASH model not only by inhibiting the TNF-alpha but also suppressing the oxidative stress markers.
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PMID:Amelioration of steatohepatitis with pentoxifylline in a novel nonalcoholic steatohepatitis model induced by high-fat diet. 1741 55

Stellate cells are activated by free radicals, and synthesize collagen. N-acetylcysteine (NAC) is a precursor of reduced glutathione and a potent scavenger of hydroxyl radicals and has potential antifibrotic effects. We aimed to test the effects of NAC on bile duct ligation (BDL) induced liver damage in rats. Forty-seven Wistar rats were divided into 5 groups: group 1, BDL+NAC (n=10); group 2, BDL (n=10); group 3, sham+NAC (n=10); group 4, sham (n=10); and group 5, control group (n=10). NAC (50 micromol/kg per day) or saline of single doses were administered intraperitoneally for 28 days. Serum biochemical and liver oxidative stress parameters were studied. Liver collagen level was determined by the method of Lopez de Leon and Rojkind. Liver slides were stained by hematoxylin and eosin and Masson trichrome\Gomory reticulum staining. Aspartate aminotransferase (AST) and alkaline phosphatase levels in the BDL+NAC group were lower than the BDL group and were higher than the control groups (all P< .001). Malondialdehyde, luminal, and glutathione levels in group 1 were lower than the BDL group (P= .01, P= .002, and P< .001) and higher than the control groups (all P< .001). NAC had no effect on alanine aminotransferase (ALT), gammaglutamyl transferase, bilirubin, albumin, or lucigenin levels. Liver collagen levels were higher in the BDL groups (P< .001); however, NAC had no effect on the collagen levels. The BDL groups showed stage 3 fibrosis; all the control groups were normal. NAC improved some biochemical parameters (AST, alkaline phosphatase) and oxidative stress parameters (malondialdehyde, luminol, glutathione) in the BDL model. NAC was found to be effective on cholestasis-induced hepatotoxicity. However, NAC was inefficient as an antifibrotic agent within a 1-month period of administration in the BDL model.
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PMID:The effects of N-acetylcysteine on bile duct ligation-induced liver fibrosis in rats. 1743 97


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