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)

Pyrazinamide (PZA) combined with either ethambutol (EMB) or a fluoroquinolone for 6-12 months is one of the treatments recommended for latent tuberculosis infection (LTBI) in contacts exposed to multidrug-resistant tuberculosis (MDR-TB). The aim of the present study was to describe the side effects related to combined PZA and EMB treatment given for LTBI, in contacts previously exposed to MDR-TB. In total, 12 consecutive contacts, all of African origin and aged 38+/-5 yrs, were treated with daily PZA (23+/-4 mg.kg(-1)) and EMB (17+/-4 mg.kg(-1)) at Geneva University Hospital outpatient clinic (Switzerland), as a result of contact-tracing procedures for two patients with contagious MDR-TB. Clinical status and liver function tests (aspartate aminotransferase (ALAT) and alanine aminotransferase (ASAT)) were monitored monthly. In seven cases (58%) treatment was discontinued after a median of 119 days, due to hepatic toxicity in six cases (ALAT or ASAT elevation more than four times the upper normal limit), and gastrointestinal symptoms in one case. In conclusion, combined pyrazinamide and ethambutol for latent tuberculosis infection may be associated with a high risk of hepatic toxicity, and warrants close monitoring. There is clearly a need for alternative preventive treatments for contacts exposed to multidrug-resistant tuberculosis.
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PMID:High hepatotoxicity of pyrazinamide and ethambutol for treatment of latent tuberculosis. 1613 29

A significant increase in plasma glutamate-oxaloacetate transaminase and glutamate-pyruvate transaminase was observed 6 h after intraperitoneal administration of D-galactosamine (D-Galn). Three hours after administration of D-Galn, the vitamin C concentration in the liver decreased significantly compared to that in a control group and thereafter the hepatic vitamin C concentration remained at a significantly lower level. Phosphorylated JNK (c-Jun NH2-terminal kinase) and phosphorylated ERK (extracellular signal-regulated kinase) started increasing 3 h after D-Galn treatment and remained at a high level for 6-12 h after the treatment, while phosphorylated p38 MAPK increased significantly 6 h after D-Galn administration. These results indicated that oxidative stress and the activation of JNK and ERK took place almost simultaneously, followed by the activation of p38 MAPK.
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PMID:Activation of mitogen activated protein kinase (MAPK) during D-galactosamine intoxication in the rat liver. 1653 Apr 10

Lamivudine treatment in hepatitis B e antigen (HBeAg)-negative and hepatitis B virus (HBV) DNA-positive chronic hepatitis B (CHB) patients is associated with poor sustained response. A previous study has shown that short-term lamivudine therapy in HBeAg-positive patients with alanine aminotransferase (ALT) > 5x upper limit of normal (ULN) could achieve a high HBeAg response rate and low lamivudine resistance rate. We, therefore, prospectively treated 85 HBeAg-negative CHB patients with ALT > 5x ULN by lamivudine for 6-12 months. The mean pretreatment levels were as follows: ALT (normal < 36 U/I) 533 U/I (range: 180-2,418 U/I); total bilirubin (normal < 1.3 mg/dl) 2.0 mg/dl (range: 0.2-29.6 mg/dl), HBV DNA (normal, undetectable) 1.6 x 10(8) copies/ml (range: 1.4 x 10(5)-1.7 x 10(9) copies/ml). After a mean of 7.4 months (6-12 months) treatment, 69 (81%) patients achieved complete response. In a follow-up, 12 months after stopping lamivudine therapy, 33 (39%) patients showed sustained complete response. Patients with sustained response were younger than the relapsed patients (39.7 +/- 11.9 years versus 47.0 +/- 10.3 years; P = 0.005). The emergence of lamivudine-resistant variant HBV was documented in two patients (2%). It is concluded that in HBeAg-negative chronic hepatitis B patients with ALT levels above 5x ULN, a 6-12 month course of lamivudine therapy may achieve sustained an off-treatment response in approximately one-third of patients.
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PMID:Short-term lamivudine therapy in HBeAg-negative chronic active hepatitis B in Taiwan. 1730 59

Thioacetamide (400 mg/kg body weight, i.p.) was administered to rats. After 12 h the activity of plasma glutamate-oxaloacetate transaminase (GOT) and glutamate-pyruvate transaminase (GPT) was significantly higher than that of the control group, and after 24 h plasma GOT and GPT activities strongly increased. These results indicated that the necrotic process was initiated at about 12 h and developed thereafter. By co-administration of dimethyl sulphoxide (DMSO, 18 and 1 h before, and 8 h after administration of thioacetamide: each time, 2.5 ml/kg body weight, p.o.), plasma GOT and GPT were significantly decreased and were even comparable to the control group, showing that DMSO totally prevented the necrotic action of thioacetamide. After 12 and 24 h of thioacetamide administration, the hepatic level of vitamin C, the most sensitive chemical indicator of oxidative stress, decreased significantly, indicating that oxidative stress was significantly enhanced 12 h after thioacetamide intoxication and thereafter. DMSO totally restored the liver vitamin C level, demonstrating that DMSO effectively ameliorated the oxidative stress caused by thioacetamide, resulting in the prevention of necrosis of the liver. Phosphorylated c-Jun NH(2)-terminal kinase (JNK) significantly increased transiently 12 h after treatment with thioacetamide. These results indicated that oxidative stress and the activation of JNK took place almost simultaneously. Phosphorylated extracellular signal-related kinase (ERK) 2 was significantly increased 6-12 h after thioacetamide injection. Phosphorylated p38 MAPK (mitogen activated protein kinase) was significantly decreased 24 h after administration of thioacetamide. DMSO treatment inhibited the change of these MAPKs by thioacetamide, corresponding with the prevention of the liver necrosis as well as the attenuation of oxidative stress.
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PMID:Effect of dimethyl sulphoxide on oxidative stress, activation of mitogen activated protein kinase and necrosis caused by thioacetamide in the rat liver. 1739 77

D-Galactosamine (D-Galn: 300 mg/kg) was intraperitoneally administered to rats. After 6 h the activity of plasma GOT and GPT was significantly higher than that of the control group and plasma GOT and GPT activities increased thereafter. These results indicated that the necrotic process was initiated at about 6 h and developed thereafter. With coadministration of DMSO (1 h before administration of D-Galn: 2.5 mL/kg, oral), plasma GOT and GPT were significantly lower, showing that DMSO inhibited the necrotic action of D-Galn. After 6-24 h of D-Galn administration, the hepatic level of vitamin C, the most sensitive indicator of oxidative stress, decreased significantly, indicating that oxidative stress was significantly enhanced 6 h after D-Galn intoxication and thereafter. DMSO significantly restored the liver vitamin C level 24 h after D-Galn injection, demonstrating that DMSO effectively ameliorated the oxidative stress caused by D-Galn, resulting in the prevention of necrosis of the liver. Phosphorylated JNK and phospho-ERK were significantly increased transiently 6-12 h after treatment with D-Galn. These results indicated that oxidative stress and the activation of JNK took place almost simultaneously. Phosphorylated p38 MAPK was not changed and DMSO treatment did not affect the change of these MAPKs by D-Galn.
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PMID:Inhibitory effect of dimethyl sulfoxide (DMSO) on necrosis and oxidative stress caused by D-galactosamine in the rat liver. 1761 4

Recent evidence indicates that inhibition of the Na+/H+ exchanger improves heart and brain injuries induced by I/R. Studies were performed to investigate whether FR183998, a Na/H exchanger inhibitor, has protective effects on hepatic I/R injury in rats. Male Sprague-Dawley rats were subjected to 70% hepatic ischemia by occluding the hepatic artery, portal vein, and bile duct associated with the left and median liver lobes with a microvascular clip for 2 h. FR183998 (1 mg/kg) was administered i.v. 10 min before the hepatic ischemia. Hepatic I/R increased the serum levels of aspartate transaminase, alanine transaminase, and lactate dehydrogenase, which peaked at 9 h after reperfusion. FR183998 reduced these injury markers and recovered liver functions. Histopathologic analysis revealed that FR183998 prevented the incidences of hepatic necrosis, apoptosis, and neutrophil infiltration at 6 and 9 h (P < 0.05). FR183998 reduced the increases in proinflammatory cytokines such as TNF-alpha (1-6 h), IL-6 (1-12 h), interferon-gamma (6-12 h), IL-1beta (1-3 h), and cytokine-induced neutrophil chemoattractant 1 (1-3 h), but enhanced the anti-inflammatory cytokine IL-10 (1 h). FR183998 inhibited the hepatic I/R-induced activation of the transcription factor nuclear factor-kappaB at 1 to 6 h and reduced the induction of iNOS at 6 to 12 h, followed by inhibition of nitric oxide production. Furthermore, FR183998 decreased the expression of the iNOS gene antisense transcript, which is involved in the stability of iNOS messenger RNA, at 9 to 12 h in the liver of hepatic I/R rats. These results demonstrate that FR183998 reduces the induction of proinflammatory cytokines and iNOS at least in part through inhibition of nuclear factor-kappaB activation and iNOS antisense transcript expression, thereby preventing hepatic I/R injury.
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PMID:Protective effect of FR183998, a Na+/H+ exchanger inhibitor, and its inhibition of iNOS induction in hepatic ischemia-reperfusion injury in rats. 1827 53

The aims of this study were to observe the relationship between injury of graft and expression of redox factor-1 (Ref-1) in early period (24 h) after liver transplantation in rat model. One hundred and fifty adult male Wister rats were randomly divided into three groups including liver transplant group, sham surgery group and untreated control group. After liver transplantation, animals were sacrificed at different time points, and the changes and significance of the expression of Ref-1 were then explored by immunohistochemistry, serology and histopathology. As compared with sham surgery group and untreated control group, the expression of Ref-1 protein in transplant group was stronger in early period after liver transplantation. With pathology analysis, lots of infiltrating inflammation cells were found around the portal veins. Hepatic tissues were injury. However, the injury in sham surgery and untreated control group were comparatively slight. The serum ALT and AST levels reached the peak at 6-12 h, and decreased significantly after 12 h. These data suggested that the degree of liver injury in earlier period after transplantation peaked at 6 h and then decreased. And Ref-1 protein induced by hepatic ischemic reperfusion injury might play a critical role in repairing the injury.
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PMID:Expression of redox factor-1 in early injury period after liver transplantation in rat model. 1972 33

The ultimate goal of treatment for chronic hepatitis B is to reduce liver-related complications and mortality. Sustained hepatitis B e antigen (HBeAg) seroconversion and hepatitis B surface antigen (HBsAg) clearance 6-12 months after stopping treatment are the short-term surrogate outcomes for interferon or peginterferon therapy. As most patients require long-term nucleos(t)ide analogue treatment, which also has the risk of drug resistance in the case of incomplete viral suppression, maintained hepatitis B virus (HBV) DNA suppression to an undetectable level is the appropriate surrogate outcome. Because no antiviral treatment is perfect, it is desirable for treatment response to be predicted and the treatment regimen modified accordingly. At baseline, high ALT and low HBV DNA levels can predict response to both (peg)interferon and nucleos(t)ide analogues. Genotype A HBV responds best to peginterferon but HBV genotype has no predictive value for nucleos(t)ide analogue treatment. HBV DNA is a good on-treatment predictor of response for nucleos(t)ide analogues but not for (peg)interferon. The data supporting the use of quantitative HBsAg and HBeAg to predict response to peginterferon is stronger than that for nucleos(t)ide analogues. In conclusion, predictors of response are useful to provide the most appropriate antiviral therapy to the most suitable patients, in order to achieve the best response and improve the clinical outcome of chronic hepatitis B patients.
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PMID:Predictors of treatment response in chronic hepatitis B. 1985 23

The aim of this work was to study specific clinical features of legionellosis pneumonia during an epidemic outbreak of the disease in Sverdlovsk region and to assess its delayed effects. 202 patients applied for the treatment to the central hospital of the town of Verkhnyaya Pyshma in July-August 2007 Legionella pneumophila was identified in 61 adults aged 51.3-59.3 (mean 55.3) years. The following analyses were performed at admittance and discharge as well as 1 year after treatment: complete blood count, urinalysis, AST, ALT and sugar levels, breast X-ray and ECG. Patients with mild disease were given azithromycin per os (500 mg for 7days, n = 10) or levofloxacin (500 mg for 10 days, n = 5). Those with the severe form of the disease were treated with azithromycin (500 mg for 3 days, v/v, n = 17) or levofloxacin (750 mg for 2-3 days v/v and for 12 days per os, n = 29). The results were analysed using the STATA 5.0 software package (Stata Corporation, College Station, Texas, USA). Difference were considered significant at p < 0.05. It was shown that the outbreak resulted from the use of hot water from the public water supply system contaminated with L. pneumophila. The incubation period of infection was 4.48-6.01 (mean 5.3) days. Duration of hospitalization varied from 9.6-12.9 (mean 11.3) days. Most common clinical symptoms: general uneasiness, headache, non-productive cough, and fever lasting 3.8-6.6 (mean 5.2 days). Intrahospital lethality 6.6%. It is concluded that therapy with azithromycin and levofloxacin give good clinical effect leaving no systemic lesions in patients with legionellosis pneumonia.
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PMID:[Clinical features and delayed aftereffects of Legionellosis pneumonia during an epidemic outbreak]. 2091 75

Rangelia vitalii is a protozoon that causes diseases in dogs, and anemia is the most common laboratory finding. However, few studies on the biochemical changes in dogs infected with this protozoon exist. Thus, this study aimed to investigate the biochemical changes in dogs experimentally infected with R. vitalii, during the acute phase of the infection. For this study, 12 female dogs (aged 6-12 months and weighing between 4 and 7 kg) were used, divided in two groups. Group A was composed of healthy dogs (n = 5); and group B consisted of infected animals (n = 7). Blood samples were collected on days 0, 10, 20 and 30 after infection, using tubes without anticoagulant to obtain serum and analyze the biochemical parameters. An increase in alanine aminotransferase (ALT) on day 20 (P < 0.05) was observed. Also, increased creatine kinase (CK) and aspartate aminotransferase (AST) levels were observed throughout the experimental period (P < 0.05). No changes in the serum gamma-glutamyltransferase, urea and creatinine levels were observed. Thus, is possible to conclude that experimental infection with R. vitalii in dogs causes changes to the biochemical profile, with increased ALT, AST and CK enzyme levels.
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PMID:Rangelia vitalii: changes in the enzymes ALT, CK and AST during the acute phase of experimental infection in dogs. 2307 Apr 34


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