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)

Fructus Schizandrae (FS) is a well-known Chinese herb which has been widely used in ancient China. During recent decades, it has been found to be effective in viral and chemical induced hepatitis. In this paper, we report the studies on the chemical constituents and pharmacological actions of FS on mice liver. The results indicated that FS and its several components can mainly protect liver from injury induced by toxic substances such as CCl4; they have anti-oxidant activities against oxygen free radicals; FS and four components have inducing action on liver cytochrome P-450; they also promote certain anabolic metabolism such as serum protein biosynthesis and glycogenesis. All these activities would be of importance in the protection and repair of the injured liver cells. The clinical use of FS is also presented.
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PMID:Pharmacological actions and clinical use of fructus schizandrae. 251 53

Furazolidone produces a dilative cardiomyopathy and hepatitis in turkeys exposed to this drug in their diets. The ability of furazolidone to enhance free radical reactions when incubated with turkey cardiac or hepatic membranes was determined to evaluate if free radical reactions might contribute to the pathology. Furazolidone (0.135 mM) incubated with NADPH and hepatic microsomes increased oxygen consumption 350% over control incubations. Superoxide dismutase and catalase attenuated the furazolidone-mediated stimulation of oxygen consumption, indicating that the drug promoted the formation of superoxide and hydrogen peroxide. Lipid peroxidation was also stimulated by furazolidone incubated with microsomes, NADPH, and ferric chloride. At concentrations as low as 0.017 mM, lipid peroxidation was more than doubled by furazolidone. Incubation of cardiac sarcosomes with NADPH and furazolidone (0.135 mM) increased oxygen consumption 72% the rate of cytochrome c reduction 72%, and epinephrine oxidation 238% over control. Epinephrine oxidation was enhanced by concentrations of furazolidone as low as 0.017 mM (69% increase over control). This effect of furazolidone was blocked by superoxide dismutase or incubation in an argon atmosphere. These data establish the potential for furazolidone to enhance free radical reactions in cardiac, as well as hepatic tissue. Free radical reactions are therefore potential determinants of furazolidone-mediated hepatic and cardiac toxicities.
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PMID:Furazolidone-enhanced production of free radicals by avian cardiac and hepatic microsomal membranes. 253 46

Three children were observed to have extensive liver injury following protracted seizures. Two recovered with supportive care and one died from central nervous system complications. When first measured, the levels of aminotransferases were minimally elevated, but they increased to 250 to 8,000 times normal within 12 to 24 h after the seizure episode. They fell to near normal over the next 8 to 11 days in the survivors, and to one sixth of the peak level by 4 days in the patients who died. A percutaneous liver biopsy from one child demonstrated centrolobular necrosis consistent with severe ischemic injury. Common causes for liver dysfunction, including viral hepatitis, drug hepatitis, and Reye syndrome, were excluded on clinical, serologic, and histologic grounds. We reason that hepatic injury resulted from ischemia. We speculate that prior treatment with anticonvulsants, which are capable of inducing mixed-function oxidases in the liver, aggravated the ischemia-reperfusion injury by increasing the production of reactive oxygen intermediates and reducing cytoprotective mechanisms. Prevention of such injury should be directed toward control of seizures and early respiratory support when seizures occur, not restructuring medication regimens.
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PMID:Acute liver injury after protracted seizures in children. 262 20

Convincing evidence is presented that oxygen free radicals are involved in the pathogenesis of rheumatoid arthritis (RA). Superoxide is produced by polymorphonuclear leucocytes (PMN) in synovial fluid and by macrophages in the synovial membrane. Tissue damage typical for free radical attack is detected in RA. No absolute deficiency of protective factors is found in RA compared to controls, but the available protection is insufficient to cope with all radicals formed. The toxicity of superoxide is increased by iron. It is doubtful whether a low molecular weight iron pool is present. Superoxide is able to release iron from ferritin, providing a suitable source of iron, for the formation of hydroxyl radicals. This new pathogenetic mechanism stimulates to the application of iron chelators in the treatment of RA. Preliminary results with desferrioxamine were disappointing because of serious side-effects. Hopefully in the future intra-articular injection of iron chelators with better pharmacodynamics will be possible. The interaction of free radicals and ferritin is probably also involved in the pathogenesis of other inflammatory diseases such as systemic lupus erythematosus, hepatitis, and haemochromatosus.
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PMID:Superoxide dependent iron release from ferritin in inflammatory diseases. 283 31

Amino sugars such as galactosamine are hepatotoxic. It has been verified that toxic hepatitis induced by galactosamine is similar to that of CCl4 poisoning, and that both were inhibited by O2* scavengers. Fructosamine results from the union of glucose with the epsilon-amine of lysine. A test for fructosamine quantification is based on nitroblue tetrazolium (NBT) reduction, in which O2- is involved, the reduction being inhibited in the presence of superoxide dismutase (SOD). Given these facts, we attempted to elucidate if galactosamine and glucosamine reduce NBT and if that reduction is inhibited by SOD. This was confirmed. Subsequently, we incubated aminoacids (glycine, lysine, alanine) with glucose and galactose for 7 days and studied the action of the incubation products on NBT, using amino acids and sugars as controls. We found that NBT reduction increases proportionally to the length of incubation time of glucose/galactose with lysine, but not with other amino acids. Reduction of NBT by the Amadori compounds formed is inhibited by SOD. We suggest that oxygen radical generation by Amadori compounds must be taken into consideration as one cause of damage in diabetes of long duration.
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PMID:Oxygen radical generation by Maillard compounds. 283 94

Medically compromised children and adults are increasingly likely to seek orthodontic care as improved medical management creates more long-term survivors. For the majority, treatment of orthodontic problems is feasible, but special precautions usually are required. These include medical consultation to establish the patient's prognosis, maintaining a current knowledge of drug therapy, and modifications in office procedures. Patients with a history of multiple transfusions should be presumed to be hepatitis carriers until proved not to be, and special precautions to protect office staff members and other patients should be taken. Decreased resistance to infection is a common complicating factor in medically compromised patients. Dentists must therefore avoid mucosal irritation and carefully monitor periodontal health. The practitioner should be alert to side effects of drug treatment such as xerostomia and depressed immune response, and be aware of the particular features of the underlying disease. Bleeding disorders, which can be managed by replacement of missing clotting factors, do not contraindicate orthognathic surgery. The major contraindication is poor anesthetic risk, which almost always is true for patients having sickle cell anemia because of poor blood oxygen saturation. Because orthodontic treatment can provide positive benefits, it should not be withheld solely because of the presence of a serious medical problem. With appropriate management, successful orthodontic treatment can be done for most patients.
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PMID:Orthodontic care for medically compromised patients: possibilities and limitations. 293 66

Free radical species are ubiquitous in plant and animal life. This article describes briefly the formation of certain oxygen-centred free radicals which are essential for aerobic metabolism and host defences in humans. The mechanism of cytotoxicity of excess or inappropriate free radical production is described. The potential relevance of free radical tissue injury to the anaesthetist is illustrated using oxygen toxicity, adult respiratory distress syndrome and halothane hepatitis as examples.
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PMID:Free radicals. Formation, function and potential relevance in anaesthesia. 259 Feb 93

Previous studies have demonstrated that sera from patients with severe liver damage after halothane anesthesia ("halothane hepatitis") contain antibodies reacting with novel antigenic determinants expressed on hepatocytes from rabbits exposed previously to halothane. To determine the structure of the halothane-induced antigen(s), immunoblotting experiments were performed using patient sera and rabbit liver subcellular fractions. Three polypeptide antigens (Mr 100,000, 76,000 and 57,000) expressed in liver fractions from animals sacrificed 16 hr after exposure to 1% halothane in oxygen for 45 min, but not in fractions from unexposed animals, were identified. Analysis of fractions prepared by differential and sucrose density gradient centrifugation, and characterized by enzyme marker analysis, localized all three antigens to a microsomal subfraction relatively enriched in glucose-6-phosphatase activity, therefore, presumably derived from the endoplasmic reticulum. Antibodies to these antigens were detected in 19 of 24 sera from patients with halothane hepatitis, and four distinct patterns of antibody specificity were observed: 100,000 + 76,000 (seven patients), 100,000 alone (seven patients), 76,000 alone (three patients) and 57,000 alone (two patients). Such antibodies were not detectable in sera from 24 normal blood donors or 36 control patients. Thus, halothane induces expression of three distinct polypeptide antigens in liver, and patients with halothane hepatitis differ in patterns of recognition of these antigens by circulating antibodies.
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PMID:Identification by immunoblotting of three halothane-induced liver microsomal polypeptide antigens recognized by antibodies in sera from patients with halothane-associated hepatitis. 330 10

In order to elucidate active oxygen in liver diseases, activities, electrophoretic profiles and immunolocalization of superoxide dismutase (SOD) in human liver specimens were investigated. Activities and electrophoresis were studied using liver homogenates in 41 cases and immunolocalization of Cu, Zn SOD was observed in 87 cases. Total SOD activity in acute viral hepatitis (AVH) and fatty liver (FL) groups was significantly lower than that in non-specific reactive hepatitis (NSRH) group. Cu, Zn SOD activity in AVH, FL and chronic active hepatitis (CAH) groups was also significantly lower than that in NSRH group. However, no difference of Mn SOD activity, was found between NSRH group and others. Decreased activity of superoxide dismutase in liver tissues suggests the release of this enzyme from the injured hepatocytes. In electrophoretic patterns of superoxide dismutase, 3 bands of Cu, Zn SOD isozymes and 8 to 10 bands of Mn SOD isozymes were recognized. Immunocytochemical investigation revealed the localization of Cu, Zn SOD in the cytoplasm of hepatocytes. Two different distribution of Cu, Zn SOD was observed in the lobules: a diffuse localization pattern and a focal one. The latter was found in the cases of liver diseases with severe parenchymal lesion. These findings suggest that superoxide radical anion and its scavenger, superoxide dismutase, may play an important role in the pathogenesis of liver cell necrosis.
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PMID:Activities, electrophoretic profiles and immunolocalization of superoxide dismutase in human liver specimens. 336 38

A guinea pig model of halothane hepatitis was used to explore the humoral immune response induced by multiple halothane exposures and the potential role this response might play in contributing to liver damage. Three different strains of guinea pigs (Strain 2, Amana, and Hartley) were exposed to 1% halothane under either 21 or 80% oxygen for 4 hr at 2-week intervals. In each strain, halothane induced the appearance of an antibody cross-reactive with trifluoroacetylated guinea pig serum albumin (TFA-GSA). Three of six Strain 2 guinea pigs demonstrated an association between antibody titer and serum glutamate pyruvate transaminase levels. However, the possible cause and effect relationship between these two factors requires more investigation. Hartley guinea pigs had a 4- to 11-fold higher level of anti-TFA antibody than the other two strains because of either a "higher responder" genetic background or exposure conditions that favored oxidative metabolism of halothane. Immunization of Amana guinea pigs with TFA-GSA evoked a specific anti-TFA antibody response. However, the presence of this antibody before halothane exposure did not potentiate the transient liver damage induced by exposure. Thus, these results demonstrate that in guinea pigs multiple exposures to halothane induce the formation of an antibody that recognizes a reactive intermediate of halothane formed during the anesthetic's metabolism.
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PMID:Generation of halothane-induced immune response in a guinea pig model of halothane hepatitis. 368 90


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