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)

Functional, biochemical and histological parameters of hepatotoxicity were assessed in male Sprague-Dawley rats receiving amiodarone (Am) short-term by gavage (5, 50, 150 and 500 mg Am kg-1 day-1, 10 days) or dietary exposure (50 ppm, 1500 ppm, 4-week duration), or by long-term dietary exposure (50 ppm, 8-month duration). Serum enzyme (ALT, AST, ICD) levels and histopathological examination indicated no observable evidence of toxicity among rats of any of the treatment groups. Reduced food intake and reduction in weight gain was observed for rats exposed short-term to 1500 ppm dietary Am. Assessment of hepatobiliary function in treated rats indicated that short-term and long-term dietary exposure to Am resulted in a compromised excretion of readily excretable phenolphthalein glucuronide (PG), although inanition may account for this effect in the 1500 ppm group. Rats receiving Am by gavage exhibited a reduction in biliary excretion of PG, which was not dose-dependent. Distribution of Am and its major metabolite, desethylamiodarone, was similar to previous reports wherein both compounds accumulated in adipose, lung and liver tissue. These data suggest that minor alterations of hepatobiliary function occur in the absence of histological alterations and may preceed biochemical changes, as assessed in this study.
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PMID:Effects of short-term and long-term administration of amiodarone on hepatobiliary function in male rats. 261 99

Female Sprague-Dawley rats (175-200 g) were maintained on a commercial powdered rat chow containing 0 or 10 ppm chlordecone (Kepone; CD). On day 15 of the dietary protocol, a single dose of CCl4 (5-100 microliters/kg) was administered i.p. in corn oil vehicle. Controls received corn oil vehicle only. Twenty-four hours after CCl4 administration, hepatotoxicity was assessed using biochemical, functional, and histopathological parameters. Serum enzymes (GPT, GOT, ICD and OCT) were elevated in a dose related manner in the animals receiving CD-CCl4 combination. CCl4 alone at the doses used had no marked effect. Centrilobular necrosis was observed in the animals receiving CD-CCl4 combination. Biliary excretion of phenolphthalein glucuronide (PG) and the rate of bile flow were decreased in a dose-dependent manner. Forty-eight hour LD50 of CCl4 was decreased 26-fold by CD pretreatment. These results indicate that CD potentiates CCl4 toxicity in female rats as well. Since the hepatic functional status is greatly compromised, the CD potentiated lethality is preceded by hepatic failure. Furthermore, female rats are sensitized to smaller doses of CCl4 in comparison to male rats.
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PMID:Potentiation of CCl4 hepatotoxicity and lethality by chlordecone in female rats. 619 Feb 68

Previous work has established the marked potentiation of CCl4 hepatoxicity by prior exposure to chlordecone (CD). This study was conducted to determine if prior exposure to CD results in enhancement of CCl4-induced destruction of the hepatic microsomal mixed-function oxygenase (MFO) system. Male Sprague-Dawley rats received a single oral dose of CD (10 mg/kg) or corn oil vehicle alone (1 ml/kg) 24 hr prior to a single ip injection of CCl4 (0-100 microliter/kg). Mirex (M; 10 mg/kg) and phenobarbital (PB; 80 mg/kg/day for two days) were used as negative and positive controls respectively for the potentiation of CCl4 hepatotoxicity. Hepatotoxicity was evaluated 24 hrs after CCl4 administration by elevations of three serum enzymes (GPT, GOT, and ICD). The key hepatic microsomal MFO parameters measured were microsomal protein, cytochrome P-450 content, glucose-6-phosphatase (G-6-Pase), and aminopyrine demethylase (APD). As previously demonstrated using a subchronic dietary pretreatment protocol, CD potentiated CCl4 hepatotoxicity over a range of CCl4 doses to a greater extent than PB or M, as judged by elevations in serum enzymes. PB caused the greatest increase in total P-450 content and the greatest increase in CCl4-mediated destruction of microsomal protein and APD activity. M caused the least destruction of total hepatic cytochrome P-450, despite the same level of cytochrome P-450 as in the PB group. CD treatment caused the greatest decrease in G-6-Pase activity in comparison to PB or M pretreatments and a similar degree of P-450 destruction as observed with the PB group. These findings suggest that in general, CCl4-induced destruction of hepatic MFO parameters measured in this study is disproportional to the known degree of potentiated hepatotoxicity by the pretreatments and does not accurately reflect the potentiation of CCl4 hepatotoxicity by CD.
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PMID:Destruction of hepatic mixed-function oxygenase parameters by CCl4 in rats following acute treatment with chlordecone, Mirex, and phenobarbital. 619 92

The propensity of chlordecone (CD) to potentiate CCl4 hepatotoxicity in rats of either sex has been well documented. The objective of the present study was to investigate the hepatotoxic effects of CD-CCl4 interaction in adrenalectomized rats. Adrenalectomized rats were maintained on 0 or 10 ppm CD and on day 15 they received a single ip injection of 25 microL CCl4/kg. Hepatotoxicity was assessed by hepatofunctional, biochemical and histopathological parameters, 24 hrs after CCl4 challenge. CCl4-induced hepatobiliary dysfunction and elevation of serum enzymes (GPT, GOT, ICD and OCT) were evident. Hepatic dysfunction was most severe in adrenalectomized rats receiving CD-CCl4 combination treatment. Histopathology of liver exhibited extensive fatty infiltration in the entire lobular structure accompanied by some necrosis. These data indicate that the capacity of CD to potentiate CCl4 hepatotoxicity is unaffected in adrenalectomized rats.
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PMID:Effect of adrenalectomy on chlordecone potentiation of carbontetrachloride hepatotoxicity. 619 34

Four population groups in Burundi were examined with respect to the following genetic markers: Hp, HbS, G6PD, 6PGD, PGM, ADA, AK, PHI, LDH, AcP, PGK, PGAM, DPGM, Dia-1, MDH, ICD, EsD, GOT and GPT. Based on the distributions of these markers a distinction could be made between 2 groups: Tutsis from Burundi and Rwanda on the one hand, and Bantus from Burundi and Zaire on the other. Some significant variations were, however, also noted inside each of these 2 groups. A factorial analysis which considered the data from a quantitative point of view confirms these conclusions.
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PMID:A study of genetic markers of the blood in four Central African population groups. 715 31

Hepatitis A viruses L-A-1 and MBB strains were attenuated by serial passages in laboratory, then appropriately attenuated strains were screened based on marmosets experiments. Three live attenuated vaccine lots L-A-1/P14, L-A-1/P21, MBB/P13 (35 degrees C) were prepared respectively. Three vaccine lots titer were 10(5.5), 10(5.0), 10(4.5) TCID50/ml. Each vaccine lot was inoculated into 2 adults and 8 children 1.0 ml intramuscularly in the upper arm. All volunteers were closely observed for 4 weeks after the inoculation: No one showed local or systemic side-effects and serum ALT, ICD were normal. Every body developed anti-HAV 2-3 weeks postinoculation. Anti-HAV IgM also seroconverted. Neutralizing antibody was detected in serum 4-6 months after inoculation. Three vaccine lots showed no significant difference in safety and immunogenicity. The experimental data showed that the live vaccines were safe and had good immunogenicity.
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PMID:[Observation of live, attenuated hepatitis A vaccines in humans]. 839 1

We conducted a prospective cohort study to describe the association between alcohol use, HIV disease progression, and drug toxicity and to determine health care provider awareness of excessive alcohol use by recruiting 881 HIV-infected veterans (median age, 49 years; 99% male; 54% African American) from 3 VA HIV clinics. Twenty percent of patients were hazardous drinkers by the Alcohol Use Disorders Identification Test, 33% were binge drinkers, 32% had a chart ICD-9 alcohol diagnosis, and 12.5% and 66.7%, respectively, were described by their health care providers as currently and ever drinking "too much." Hazardous/binge drinkers more often had detectable viral loads (P < 0.001). Patients with alcohol diagnoses more often had elevated alanine transaminase or aspartate transaminase levels (P </= 0.02), anemia (P < 0.001), and elevated mean corpuscular volume (P < 0.001). Health care providers missed hazardous drinking in patients with undetectable viral loads (P = 0.01), patients without hepatitis C (P = 0.09), and patients with normal aspartate transaminase levels (P = 0.07) and missed alcohol diagnoses in patients without hepatitis and those with CD4 cell counts of >200/mL. We conclude that in HIV-positive veterans, hazardous drinking and alcohol diagnoses were common and associated with HIV disease progression and/or hepatic comorbidity and anemia. Health care providers more often missed alcohol problems in patients with less severe HIV infection and those without evidence of liver disease. Health care providers should routinely screen and counsel patients regarding alcohol problems as part of standard of care to minimize disease progression and bone marrow and hepatic toxicity.
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PMID:How harmful is hazardous alcohol use and abuse in HIV infection: do health care providers know who is at risk? 1286 42

Approximately 3.2 million persons are chronically infected with the hepatitis C virus (HCV) in the U.S.; most are not aware of their infection. Our objectives were to examine HCV testing practices to determine which patient characteristics are associated with HCV testing and positivity, and to estimate the prevalence of HCV infection in a high-risk urban population. The study subjects were all patients included in the baseline phase of the Hepatitis C Assessment and Testing Project (HepCAT), a serial cross-sectional study of HCV screening strategies. We examined all patients with a clinic visit to Montefiore Medical Center from 1/1/08 to 2/29/08. Demographic information, laboratory data and ICD-9 diagnostic codes from 3/1/97-2/29/08 were extracted from the electronic medical record. Risk factors for HCV were defined based on birth date, ICD-9 codes and laboratory data. The prevalence of HCV infection was estimated assuming that untested subjects would test positive at the same rate as tested subjects, based on risk-factors. Of 9579 subjects examined, 3803 (39.7%) had been tested for HCV and 438 (11.5%) were positive. The overall prevalence of HCV infection was estimated to be 7.7%. Risk factors associated with being tested and anti-HCV positivity included: born in the high-prevalence birth-cohort (1945-64), substance abuse, HIV infection, alcohol abuse, diagnosis of cirrhosis, end-stage renal disease, and alanine transaminase elevation. In a high-risk urban population, a significant proportion of patients were tested for HCV and the prevalence of HCV infection was high. Physicians appear to use a risk-based screening strategy to identify HCV infection.
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PMID:Hepatitis C testing practices and prevalence in a high-risk urban ambulatory care setting. 2049 11

Nonalcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease in children and adolescents. The goal of this study was to describe the demographic, anthropometric and biochemical data of children and adolescents diagnosed with NAFLD during a seven-year period in an outpatient pediatric clinic in the Southwest region of the US and to evaluate relationships between race, BMI, ALT, triglyceride levels, age and gender with a diagnosis of NAFLD. A retrospective medical record review of patients who attended an outpatient pediatric clinic with a billing diagnosis ICD-9 code of 571.8 was conducted. Forty-one patients met these criteria. The majority was male (74%) Hispanic (32%), Hispanic/Latino (68%) and obese. The small number of patients diagnosed with NAFLD in our study is consistent with previously reported results. Our results indicate that the population of this culturally diverse, high-risk population has significant clinical markers that are indicative of NAFLD.
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PMID:Relationships Between Alanine Aminotransferase, Serum Triglycerides, Body Mass Index and Nonalcoholic Fatty Liver Disease in an Outpatient Pediatric Clinic Population. 2669 Jul 17