Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immediate attention must be given to the respiratory system of the heroin abuser; then he should be given naloxone HCl. Search for evidence of use of additional drugs, which may compound problems. Pulmonary edema, aspiration pneumonia and pulmonary embolization are the most common complications. Infections, particularly endocarditis, and cardiac arrhythmia also occur with heroin overdose. Hepatitis is common. Treatment must include not only attention to the presenting symptoms but also referral to a rehabilitation center when possible.
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PMID:Treating heroin overdose. 112 10

In adrenalectomized female rats a single dose of 375 mg D-galactosamine.HCl per kg of body weight produces both hepatitis and generalized edema with ascites. These alterations depend upon the dose and the time interval after injection of the aminosugar. The effect is specific for D-galactosamine; 2-deoxy-galactose produces only edema and no hepatitis, whereas D-glucosamine and D-galactose are without any measurable effect. In male adrenalectomized animals D-galactosamine produced hepatitis alone; fluid extravasation occurs only after additional orchiectomy. Glucocorticoids given before or simultaneously with D-galactosamine are able to prevent the animals from gettin edema and to ameliorate hepatitis, while mineralcorticoids do not show any effect on these alterations. It is evident that the effects of D-galactosamine on the hepatocyte and on the endothelial cells are independent from each other. This leads to the conclusion that D-galactosamine acts at least upon two different target organs, the liver and the reticulo-endothelial system in general.
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PMID:The appearance of D-galactosamine-induced hepatitis and generalized edema in adrenalectomized rats. 118 Aug 18

Disordered gustatory acuity was demonstrated in 22 patients with acute viral hepatitis and in 16 patients with chronic liver disease utilizing subjective responses and objective measurements of detection and recognition thresholds and scaling for NaCl, sucrose, HCl, and urea. In patients with early hepatitis and those with chronic liver disease, the magnitude and the uniformity of the threshold elevations were comparable, implying that disordered gustatory acuity reflects disordered hepatic function per se. Patients with acute hepatitis showed a significant fall in taste thresholds (improvement in acuity) as the hepatitis waned, indicating that the gustatory defect is reversible. This disorder of gustatory acuity may contribute to the anorexia commonly found in patients with liver disease.
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PMID:Disordered gustatory acuity in liver disease. 125 40

1,2-Dimethylhydrazine-HCl (DMH-2HCl) is derived from the natural toxin cycasin, and is extensively used to induce cancers in experiments with rodents. We examined the toxicity of DMH-2HCl, incorporated into purified diets varying in protein, to determine concentrations compatible with long-term survival in B6C3H1 mice. Initial studies showed single-dose oral LD50 values (95% confidence intervals) of 26 (18-32) mg DMH-2HCl/kg body weight for males, and 60 (53-65) for females. A 6-wk study was performed with diets containing 10 or 40% soybean protein with doses of 0, 11.25, 22.5, 45, 90, and 180 mg DMH-2HCl/kg diet. All mice fed the highest dose were removed from the study due to severe toxicity. Declines in food consumption and body weight occurred in both sexes, accelerated with increasing log(DMH) dose, and were substantially more severe in groups fed 10% protein. A 5-mo study was subsequently performed with male mice fed 10 or 40% protein diets containing doses of 0, 15, 30, or 45 mg DMH-2HCl/kg diet. In this longer study, dose-related declines of food intake and body weight were also more pronounced with 10% protein. Histopathologic examination of samples from 29 organs/tissues revealed hepatic changes most commonly, and these were more severe at higher DMH levels. Lesions ranged from focal centrilobular hepatocellular necrosis to severe toxic hepatitis, associated with lobular disorganization and hepatocellular hypertrophy. Frequent dose-dependent lesions were also found in kidneys, adrenals, and heart. Renal changes included focal subcapsular fibrosis with atrophy, and hyperplasia of the tubular epithelium. Adrenal cortical hypertrophy was noted at the two highest DMH doses. Focal cardiac myocytolysis was also noted at high DMH doses. Renal damage occurred only rarely in the absence of liver pathology, and adrenal hypertrophy only rarely without renal damage. Cardiac myocytolysis was found in 14% of mice without hepatic, renal, or adrenal damage, but in 62% of those with lesions in each of those organs. No evidence of gastrointestinal toxicity was observed. Hepatic, renal, and adrenal lesions were more frequent and severe in mice fed the low-protein diet. The protective effect of high protein was DMH-dose dependent. The lower doses in these studies could be used to investigate effects of diet, cocarcinogens, or chemopreventative agents on carcinogenesis resulting from chronic, low-level dietary exposure to DMH.
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PMID:Dietary protein and chronic toxicity of 1,2-dimethylhydrazine fed to mice. 201 52

The polymerase chain reaction (PCR) technique has been utilized for the detection of hepatitis B virus (HBV) DNA, and several factors related to the selection of primer pairs for the PCR amplification have been demonstrated. The sensitivity of the PCR assay was compared with that of slot-blot hybridization for detecting HBV-DNA. Analysis by the PCR technique with Southern blot hybridization provided a greater than 10(4)-fold increase in sensitivity over the slot-blot hybridization analysis. Also, a rapid and sensitive PCR method for the detection of serum HBV-DNA was developed: HBV-DNA is released from virions by incubating serum with NaOH followed by neutralization with HCl. HBV-DNA sequences are then detected by agarose gel electrophoresis and ethidium bromide staining after PCR amplification with successive sets of primer pairs. In testing serial samples from chimpanzees experimentally infected with HBV, HBV-DNA was detected 2-3 wk before the appearance of hepatitis surface antigen (HBsAg) and continued to be detectable for a short period after the production of antibody to HBsAg. Results from testing of human serum demonstrated that the majority of patients with HBsAg in serum had HBV-DNA as well and that some patients had HBV-DNA in serum in the absence of HBsAg.
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PMID:Detection of hepatitis B virus DNA using the polymerase chain reaction technique. 228 67

The following procedure for the detection of non-acetylated amino sugars in the plasma membrane was established: i) derivatization of free amino groups with dansyl-chloride, ii) hydrolysis with 3 M HCl (for 4 h at 105 degrees C) to liberate the dansylated carbohydrate moieties from the plasma membrane, iii) purification of the dansylated amino sugars by paper chromatography and subsequent analysis by thin-layer chromatography. Using this procedure, plasma membranes from rat liver were analysed after injection of D-[14C]galactosamine. For this purpose, rats were divided into three groups: the first received D-galactosamine.HCl at a dose of 2 mg/kg b.w., the second at a dose of 75 mg/kg b.w. and the third at a hepatitis-inducing dose of 260 mg/kg b.w.. In all three groups the majority of the protein-bound radioactivity in the plasma membrane was not dansylated, thus representing N-acetylated amino sugars. At a dose of 2 mg/kg, only 0.34% of the protein-bound radioactivity in the plasma membrane reacted with dansyl-chloride. At a dose of 70 mg/kg this value increased to 1.9%. At 260 mg/kg the value was 3.6%. These results indicate that the incorporation of non-acetylated amino sugar into the plasma membrane was dose-dependent and reached 90 pmol per mg plasma membrane protein during galactosamine injury. However, this incorporation of non-acetylated amino sugars into the plasma membrane did not represent a pathological mechanism responsible for the onset of the galactosamine-induced liver injury.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Incorporation of non-acetylated hexosamines into plasma membrane glycoproteins of liver cells after galactosamine injection. 322 92

Hepatitis was induced in rabbits by a single intraperitoneal injection of D(+)-galactosamine-HCl (750 mg/kg body wt). Plasma lecithin:cholesterol acyltransferase activity fell to 5% and lipid transfer protein activity to 50% of control values 48 hr after injection. Discoid high density lipoprotein began to appear in plasma of treated rabbits 36 hr after injection, along with populations of high density lipoprotein (HDL) which were both smaller (radius 3.7 nm) and larger (radius 5.9 nm) than the original HDL population (radius 4.8 nm).
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PMID:D-galactosamine induced hepatitis in the rabbit: effect on lecithin:cholesterol acyltransferase activity, plasma lipid transfer protein activity and high density lipoproteins. 379 65

The present study was carried out to examine the effect of single or consecutive administration of T-2588 on liver of male rat injured by the administration of D-galactosamine X HCl. The T-2588 was orally given to hepatic-injured rats at doses of 125 mg/kg and 1,000 mg/kg singly or for consecutive 5 days. A 10 ml/kg dose of the vehicle was orally given to control rats. The results obtained were summarized below. Single administration of T-2588. Twenty-four hours after a single administration of T-2588, the liver taken from control rats apparently indicated galactosamine-induced hepatitis. No drug-related alterations were observed in hepatic functional test, liver weight and histological examinations at either dose of T-2588. Galactosamine-induced hepatitis was not affected by a single administration of T-2588. Consecutive administration of T-2588. Twenty-four hours after a 5-consecutive-day administration of T-2588, galactosamine-induced hepatitis in control rats was restored to the normal state. The cure of galactosamine-induced hepatitis was not affected by a 5-consecutive-day administration of T-2588. The hepatic aldehyde dehydrogenase activity in hepatic-injured rats was not affected by a 5-consecutive-day administration of T-2588.
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PMID:[Effect of single or consecutive administration of T-2588 on hepatic-injured male rats]. 379 80

Thymectomized DBA/2 mice, irradiated with 720 rad/min and reconstituted with syngeneic bone marrow, were treated i.p. with 1 g/kg body weight D-galactosamine-HCl (DGA). Light and electron microscopic changes characteristic of the toxic effect of the agent, such as hepatocellular cytoplasmic inclusions and unicellular necrosis, could be observed but no inflammatory reaction was detectable in the liver. The phagocytic activity of Kupffer cells proved to be unchanged in immunosuppressed animals. Liver regeneration following DGA injury took place in 120 hours exactly as in animals having an intact immune system. The experiments suggested that T-lymphocytes participate in the development of DGA-hepatitis and their absence does not influence the restoration of liver injury. The experimental system described seems to be suitable for separating primary and secondary events and also for studying the role of the immune system in toxic liver injury.
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PMID:D-galactosamine-induced liver injury in immunosuppressed mice. 608 23

This study was undertaken to determine the effects of two H2-receptor antagonists, cimetidine and ranitidine, on halothane metabolism and hepatotoxicity in the hypoxic Fisher 344 rat model for halothane hepatitis. In this model, liver injury is caused by toxic intermediates formed during metabolism of halothane by a reductive pathway. Administration of cimetidine (120 mg/kg ip) 20 min prior to anesthesia led to inhibition of the reductive pathway, as assessed by measurement of the exhaled metabolites, 2-chloro-1,1,1-trifluoroethane and 2-chloro-1,1-difluoroethylene, during anesthesia, and urinary fluoride excretion in the 22-hr postanesthesia period. Oxidative metabolism of halothane, assessed by serum bromide concentrations 22 hr postanesthesia, was unaffected. Cimetidine administration provided partial protection against the hepatotoxic effect of halothane, as indicated by serum alanine aminotransferase activities 22 hr postanesthesia. When ranitidine HCl (120 mg/kg ip) was administered prior to anesthesia, reductive metabolism of halothane was unaffected, but the oxidative pathway was slightly inhibited. Ranitidine did not provide protection against halothane-induced liver injury. These results provide additional evidence that halothane hepatotoxicity in the hypoxic rat model is due to toxic intermediates formed during the reductive metabolism of halothane.
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PMID:Effects of cimetidine and ranitidine on halothane metabolism and hepatotoxicity in an animal model. 614


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