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At least 19 recordsLinked to original sources
PubMed2000

Effects of cAMP-dependent protein kinase and ATP on N1-oxidation of 9-benzyladenine by animal hepatic microsomes.

N1-Oxidation is a major metabolic pathway for 9-benzyladenine (BA) catalyzed by the cytochrome P450 system in animal hepatic microsomes. After normal hamster hepatic microsomes or phenobarbital induced rabbit hepatic microsomes were preincubated in the presence of cyclic AMP-dependent protein kinase catalytic subunit (PKA), MgCl2 and ATP, BA-N1-oxidation was significantly decreased. However, further investigation indicated that the decrease of BA-N1-oxidation seemed to be a combination of the effects of PKA and ATP, as ATP alone showed a biphasic regulatory effect on BA-N1-oxidation when microsomes were preincubated in the presence of various concentrations of ATP. In the lower ATP concentration range (0.5-2.5mM), BA-N1-oxidation increased along with the increase of ATP concentration; whereas BA-N1-oxidation decreased when the ATP concentration was higher (>5mM). The biphasic regulatory effects of ATP on BA-N1-oxidation seem dependent on the incubation process, as preincubation markedly strengthened the effects. When microsomes were incubated at 37 degrees C for different time lengths in the absence or presence of ATP (2.5 or 20mM), the activity of BA-N1-oxidase decreased at similar rates in all groups, but the activity levels of BA-N1-oxidase were different among the groups. The cytochrome P450 content was not changed parallel to the variation of BA-N1-oxidation when microsomes were incubated in the presence of ATP, indicating that the effects of ATP on BA-N1-oxidation were not mediated by affecting CYP stability. In addition, the activity of NADPH-cytochrome P450 reductase was not markedly affected by ATP without incubation. The result implied that ATP did not inhibit the reductase directly. After microsomes were incubated in the presence of low ATP concentration (2.5mM), the reductase was slightly inhibited, whilst high ATP concentration (20mM) showed marked inhibition (83% of control). This may partially contribute to the down-regulatory effect of ATP on BA-N1-oxidation. Furthermore, it was found that the presence of magnesium ions during preincubation weakened the up-regulatory effect of ATP (2.5mM) on BA-N1-oxidation, but showed no effect on the down-regulatory effect of ATP (20mM). Since these observed phenomena are not readily explained, a possible mechanism, i.e. phosphorylation and dephosphorylation of cytochrome P450, is suggested.

Adenine↗
PubMed1976

Infectious canine hepatitis: animal model for viral-induced disseminated intravascular coagulation.

The objective of this study was to characterize the hemostatic defect in dogs with infectious canine hepatitis (ICH), a naturally occurring viral disease of dogs. Five littermate dogs were inoculated with 10(3) TCID50 of ICH virus intravenously. Two littermates were controls. The clinicopathologic manifestations of ICH were fever, depression, anorexia, hematemesis, melena, widespread mucocutaneous petechiae, prolonged bleeding from venipunctures, faceial edema, leukopenia, and proteinuria. The hemostatic defect of ICH was characterized by thrombocytopenia, abnormal platelet function, prolonged one-stage prothrombin time and activated partial thromboplastin time, normal thrombin times, depressed factor VIII activity, and increased fibrin-fibrinogen degradation products. These findings suggested that the central pathologic mechanism of the abnormal hemostasis in ICH was disseminated intravascular coagulation (DIC). ICH is an example of DIC induced by viral infection. This disease is a suitable model for investigation of the detection, pathogenesis, and therapy of DIC.

Animals↗
PubMed1990

Endogenous benzodiazepine receptor ligands in human and animal hepatic encephalopathy.

The role of endogenous benzodiazepine receptor ligands in the pathogenesis of hepatic encephalopathy was studied in humans and in rat models of hepatic encephalopathy. Endogenous benzodiazepine ligands were extracted from rat brain and human CSF by acid treatment and purification by HPLC. Detection and partial characterization of these endogenous benzodiazepine ligands were carried out using both radioreceptor binding assays and radioimmunoassays with anti-benzodiazepine antibodies. Four different benzodiazepine receptor ligands were identified in human and rat tissue, two of which may be diazepam and desmethyldiazepam, based on elution profiles and anti-benzo-diazepine antibody reactivity. Human CSF and serum from patients with hepatic encephalopathy contained approximately 10 times more endogenous benzodiazepine receptor ligand than CSF from controls or nonencephalopathic patients with liver disease. The levels of brain benzodiazepine receptor ligand compounds were also increased approximately 10-fold in rats suffering from fulminant hepatic failure, but not in rats with portacaval shunts, a model of chronic hepatic disease. The increased concentrations of these substances could be behaviorally significant and may contribute to the pathogenesis of hepatic encephalopathy.

Adult↗
PubMed1993

Identification of the human and animal hepatic cytochromes P450 involved in clonazepam metabolism.

This report characterizes the cytochrome P450 isozyme involved in clonazepam metabolism. This study was undertaken using a library of liver microsomal fractions prepared from untreated rabbits or those treated with drugs known to specifically induce various cytochrome P450 isozymes (ie P450 2B4 by phenobarbital, P450 1A1 and P450 1A2 by 3-methylcholanthrene and beta-naphthoflavone, P450 2E1 by acetone and ethyl alcohol, and P450 3A6 by erythromycin). Only microsomes obtained from phenobarbital-treated rabbits exhibited a type II binding spectrum upon addition of clonazepam (Ks(app) = 31.4 +/- 3.8 microM) and significantly metabolized clonazepam to 7-aminoclonazepam. Benzphetamine, which is a known substrate for P450 2B1 was also extensively metabolized by microsomes prepared from phenobarbital treated rabbits. This indicates that the same isozyme (P450 2B subfamily) was involved in the biotransformation of both substrates. Experiments performed on 14 human liver microsomal preparations showed a wide interindividual variability (from 1-4) and a good correlation (r = 0.70) between benzphetamine and clonazepam metabolism. Since P450 3A4 (nf25) was involved in benzphetamine metabolism, clonazepam was probably nitroreduced by the same isozyme. An oligonucleotide specific for the P450 3A4 gene subfamily was synthetized and used for hybridization on total RNA from human liver samples. Two transcripts of 2.2 and 3.0 kb were detected and the level of the 2.2 kb mRNA expression was significantly correlated (r = 0.61) with the intensity of clonazepam nitroreduction by the corresponding microsome batches.

Animals↗
PubMed1992

Enteric non-A, non-B hepatitis: epidemics, animal transmission, and hepatitis E virus detection by the polymerase chain reaction.

We studied epidemics of viral hepatitis occurring at three different places in India. One was a combined epidemic due to hepatitis E virus (HEV) and hepatitis A virus (HAV) infections. In this epidemic, HAV affected children below 10 years of age, whereas HEV infected the young adult population. HEV was transmitted to rhesus monkeys (Macaca mulata) and confirmed by the polymerase chain reaction (PCR) on bile from the animals. Fecal material from acutely infected patients in one of the epidemics was also found positive for HEV RNA by PCR. This may help in confirming the nature of future epidemics. The bile and liver from experimental animals can be used as a source of material for further virological and molecular biological studies of HEV.

Adolescent↗
PubMed1993

The role of endogenous benzodiazepines in hepatic encephalopathy: animal studies.

Hepatic encephalopathy (HE) resembles encephalopathies induced by drugs, including benzodiazepines (BZs), that potentiate GABAergic neurotransmission. Neurons from animals with HE show increased sensitivity to BZ and GABA receptor agonists. Moreover, these neurons are excited by BZ receptor antagonists at concentration that do not affect control neurons. In addition, elevated levels of 1,4-BZs, including diazepam and N-desmethyldiazepem, have been found in the brains of animals with HE. Furthermore, behavioral and electrophysiologic ameliorations of HE have been induced in animals by BZ receptor antagonists. These findings suggest that endogenous BZs contribute to the manifestations of HE by augmenting GABAergic neurotransmission.

Animals↗
PubMed2004

Hepatitis E viruses in humans and animals.

Hepatitis E virus (HEV) is an emerging pathogen belonging to a newly recognized family of RNA viruses (Hepeviridae). HEV is an important enterically transmitted human pathogen with a worldwide distribution. It can cause sporadic cases as well as large epidemics of acute hepatitis. Epidemics are primarily waterborne in areas where water supplies are contaminated with HEV of human origin. There is increasing evidence, however, that many animal species are infected with an antigenically similar virus. A recently isolated swine virus is the best candidate for causing a zoonotic form of hepatitis E. The virus is serologically cross-reactive with human HEV and genetically very similar, and the human and swine strains seem to be cross-infective. Very recent evidence has also shown that swine HEV, and possibly a deer strain of HEV, can be transmitted to humans by consumption of contaminated meat. In this review, we discuss the prevalence, pathogenicity, diagnosis and control of human HEV, swine HEV, the related avian HEV and HEV in other hosts and potential reservoirs.

Animals↗
PubMed2001

Compromised hepatic detoxification in companion animals and its correction via nutritional supplementation and modified fasting.

Dietary components play a crucial role in the health of companion animals, especially those exposed to elevated levels of toxins and free radicals. Investigation into animals' hepatic antioxidant and metabolite conjugation systems, and the metabolic processes that influence them, provides some understanding regarding the relationship of diet to disease prevention and treatment. A review of current literature and research publications suggests nutritional supplementation can be an effective treatment for animals suffering from increased oxidative stress and toxicity. The results of recent in vivo assessments, clinical trials, and observational studies show oral supplementation with vitamin E, selenium, glutathione, and taurine to be beneficial for both maintaining natural antioxidant systems and protecting against a number of degenerative diseases associated with free radical damage and toxin exposure. In many instances, it has been observed that the introduction of specific nutrients positively influences the health status, symptomatic presentation, and life span of animals whose natural detoxification systems are compromised.

Animal Nutritional Physiological Phenomena↗
PubMed1991

Hepatitis delta virus cDNA sequence from an acutely HBV-infected chimpanzee: sequence conservation in experimental animals.

Hepatitis delta virus (HDV) RNA was isolated from the serum of a chimpanzee acutely infected with hepatitis B virus (HBV) and superinfected with HDV. Interference of HDV with HBV resulted in decreased HBV DNA levels in the serum. This interference did not change the size of the two HBV specific RNAs present in the liver of the chimpanzee. The complete cDNA sequence of the HDV RNA (5th passage) was determined. Comparison of this cDNA sequence with our previously published sequence (4th passage), located in the variable domain of HDV, was highly conserved. The HDV strain used for these infections originated from a human HDV isolate also used for five to seven HDV passages in chronic HBV carrier chimpanzees (subtypes adw and ayw) or woodchucks chronically infected with woodchuck hepatitis virus (WHV). The complete HDV cDNA sequence showed an extreme conservation (up to 99.8% homology) with the previously published animal-derived HDV cDNA sequences irrespective of passage number and animal species. In contrast a markedly lower homology (85-89%) was found when compared with 3 human-derived HDV cDNA sequences. Comparison of our complete cDNA sequence with the human-derived cDNA sequences showed that the nucleotide changes in the human-derived isolates were restricted to specific regions on the genome and to specific basepair substitutions. The hepatitis Delta antigen (HDAg) is highly conserved both in the human- and animal-derived cDNA sequences showing mainly conservative amino acid changes.

Acute Disease↗
PubMed1995

The relationship between plasma and brain quinolinic acid levels and the severity of hepatic encephalopathy in animal models of fulminant hepatic failure.

Quinolinic acid is an excitatory, neurotoxic tryptophan metabolite proposed to play a role in the pathogenesis of hepatic encephalopathy. This involvement was investigated in rat and rabbit models of fulminant hepatic failure at different stages of hepatic encephalopathy. Although plasma and brain tryptophan levels were significantly increased in all stages of hepatic encephalopathy, quinolinic acid levels increased three-to sevenfold only in the plasma, CSF, and brain regions of animals in stage IV hepatic encephalopathy. Plasma-CSF and plasma-brain quinolinic acid levels in rats and rabbits with fulminant hepatic failure were strongly correlated, with CSF and brain concentrations approximately 10% those of plasma levels. Moreover, there was no significant regional difference in brain quinolinic acid concentrations in either model. Extrahepatic indoleamine-2,3-dioxygenase activity was not altered in rats in stage IV hepatic encephalopathy, but hepatic L-tryptophan-2,3-dioxygenase activity was increased. These results suggest that quinolinic acid synthesized in the liver enters the plasma and then accumulates in the CNS after crossing a permeabilized blood-brain barrier in the end stages of liver failure. Furthermore, the observation of low brain concentrations of quinolinic acid only in stage IV encephalopathy suggests that the contribution of quinolinic acid to the pathogenesis of hepatic encephalopathy in these animal models is minor.

Animals↗