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)

Recent crystallographic and functional analyses of RNA enzymes have raised the possibility that the purine and pyrimidine nucleobases may function as general acid-base catalysts. However, this mode of nucleobase-mediated catalysis has been difficult to establish unambiguously. Here, we used a hyperactivated RNA substrate bearing a 5'-phosphorothiolate to investigate the role of a critical cytosine residue in the hepatitis delta virus ribozyme. The hyperactivated substrate specifically suppressed the deleterious effects of cytosine mutations and pH changes, thereby linking the protonation of the nucleobase to leaving-group stabilization. We conclude that the active-site cytosine provides general acid catalysis, mediating proton transfer to the leaving group through a protonated N3-imino nitrogen. These results establish a specific role for a nucleobase in a ribozyme reaction and support the proposal that RNA nucleobases may function in a manner analogous to that of catalytic histidine residues in protein enzymes.
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PMID:General acid catalysis by the hepatitis delta virus ribozyme. 1640 82

A method is developed of kryopreservation of a liquid virus vaccine against duck hepatitis virus in liquid nitrogen at -196 degrees C or in its pairs (-168 to - 175 degrees C) with the subsequent fast defreezing on water bath at 40 degrees C within 2 minutes allowing to keep to initial property of a vaccine within 2 years (the period of supervision) and the rules of vaccine lyophilization with application of three-component protective environment, with 6% of peptone, 4.8% of sorbite, 1% of gelatin with sublimation chamber temperature no less than -40 degrees C in the first 4 h of lyophilization ensuring prolongation of storage term of the a liquid vaccine from 6 months in conditions of hypothermic storage (4-8 degrees C) to one year in the dried up condition.
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PMID:[Development of the methods of cryopreservation and lyophilization of vaccine against duckling hepatitis virus from "K-IP" strain]. 1710 Mar 32

Several studies have investigated the role of neutrophils during endotoxin-mediated liver injury, yet the precise mechanism for endotoxin-mediated hepatic neutrophil transmigration is unknown. The primary objective of this study was to establish a reliable lipopolysaccharide (LPS)-mediated necro-hepatitis model to investigate the mechanisms of hepatic neutrophil infiltration following LPS administration. Male Sprague Dawley rats were administered a single (5 or 10 mg kg(-1), i.v.) or repeated injection of LPS (10 mg kg(-1), i.v., 24 h apart) with appropriate controls (i.v. saline) and were killed at various time points following LPS injection. Significant hematologic changes included neutrophilia, elevation of the neutrophil to lymphocyte ratio and toxic changes in neutrophils. Biochemical changes were observed in several liver (aspartate aminotransferase AST, gamma glutamyl transferase GGT) and kidney (blood urea nitrogen BUN) associated parameters generally at the earliest time points. Histopathology revealed a time-dependent neutrophil and mononuclear infiltration around the periportal areas in the single dose study and multifocal midzonal coagulative necrosis in the repeated dose study. The neutrophil adhesion molecule, CD 11b was up-regulated in single and repeat dose studies. Based on these studies, a reliable LPS-mediated hepatitis model with necrosis was developed by intravenous administration of LPS in a repeat dose fashion. Midzonal hepatic necrosis, peripheral neutrophilia, hepatic neutrophil infiltration and up-regulation of CD11b were the most significant and consistent markers of LPS mediated effects in this model.
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PMID:Characterization of a lipopolysaccharide mediated neutrophilic hepatitis model in Sprague Dawley rats. 1737 Feb 40

Rabbit hemorrhagic disease virus (RHDV) induced viral fulminant hepatitis in adult rabbits. We investigated the damage of renal function and electrolyte balance in experimentally infected rabbit by measuring the related serum parameters to elucidate the pathogenesis of RHDV as an index for medical treatment. Nineteen New Zealand White rabbits, ten females and nine males, were each intramuscularly inoculated with 0.5 ml 50% rabbit lethal dose (RLD(50)) rabbit hemorrhagic disease virus. Blood samples were collected at 0 hr post inoculation (HPI) and every 6 hr from 18 HPI repeatedly through 66 HPI. After virus inoculation, serum blood urea nitrogen (BUN), creatinine (CREA) and sodium (Na(+)) were elevated to a highly significant level (p<0.0001), whereas serum potassium (K(+)) was moderately elevated to a significant level (p<0.05). Hypoglycemia developed highly significantly (p<0.0001). Serum chloride ion (Cl(-)) was the only parameter which did not change significantly (p=0.077). No significant sexual difference was observed among these parameters. Renal insufficiency progressed from 36 hr, as indicated by the increases in BUN and CREA; significant changes in electrolytes resulting in the increased osmolality of extracellular fluid that induced flow disturbance which consequently destroy the homeostasis in cells. Therefore, the later impairments in renal function and electrolyte balance might be an important threat for rabbits which might have survived from acute fulminant hepatitis in RHD.
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PMID:Impairment of renal function and electrolyte balance in rabbit hemorrhagic disease. 1884 Sep 70

The effects of lactic acid bacteria-fermented soybean extract (Biofermentics; BF) on experimental models of hepatic and renal disorders were investigated in vivo and in vitro. In rat, hepatitis induced by feeding of deoxycholic acid (DCA, 0.5 wt/wt, n = 6) or intraperitoneal injection of d-galactosamine (GMN, 500 mg/body wt, n = 6), the increase in serum AST (aspartate aminotransferase) and ALT (alanine aminotransferase) levels were inhibited significantly (P < 0.05) by feeding a diet containing 5% dried BF. Moreover, the BF-administered rat group showed lower concentrations of blood urea nitrogen and a larger amount of urine as compared with values in the control group. Pretreatment of primary cell cultures of rat hepatic and renal cells with BF prior to exposure to dichromate (K(2)Cr(2)O(7)) resulted in a marked decrease of dichromate-induced cytotoxicity as evaluated by the leakage of lactate dehydrogenase The levels of dichromate-induced lipid peroxidation, as monitored by malondialdehyde formation, were also reduced by pretreatment of hepatocytes with BF. These results suggest that BF may play a role in hepatic and renal disorders, and may be useful for maintaining health in humans as well.
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PMID:Improvement of Experimentally Induced Hepatic and Renal Disorders in Rats using Lactic Acid Bacteria-fermented Soybean Extract (BiofermenticsTM). 1895 65

The adverse events of the nitrogen-containing bisphosphonates are reviewed. Oral bisphosphonates (alendronate, risedronate and ibandronate), mainly used for the treatment of osteoporosis, have been associated with adverse events from the upper gastrointestinal tract, acute phase response, hypocalcaemia and secondary hyperparathyroidism, musculoskeletal pain, osteonecrosis of the jaw and ocular events. Intravenous bisphosphonates (pamidronate, ibandronate and zoledronic acid), used in oncology and for the treatment of osteoporosis, have been associated with all the above adverse events, except those from the upper gastrointestinal tract. Moreover, pamidronate and zoledronic acid have been associated with renal toxicity. Association of bisphosphonates with atrial fibrillation and atypical fractures of the femoral diaphysis remains uncertain. There are a few case reports relating bisphosphonates to cutaneous reactions, oral ulcerations, hepatitis and esophageal cancer. Generally, intravenous are more potent than oral bisphosphonates and the frequency and severity of some of the bisphosphonate- associated adverse events are dose and potency dependent.
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PMID:Bisphosphonate-associated adverse events. 1957 Jul 37

We have shown that direct reaction of catechol with nitric oxide (NO) results in generation of reactive oxygen and nitrogen species (RNS) through semiquinone radical formation, leading to oxidative DNA damage in rat forestomach. In the present study, we investigated whether dietary catechol systemically exerts the same effects under NO-rich circumstances, when given before and during induction of inflammatory lesions. Male ICR mice were treated with or without 0.8% catechol in the diet for 2 weeks followed by acetaminophen (APAP) administration at a dose of 300mg/kg by single i.p. injection. Along with several indicators of APAP-induced hepatitis, 8-hydroxydeoxyguanosine (8-OHdG) levels and immunohistochemistry for 3-nitrotyrosine (NO(2)Tyr) in the livers were examined at 1.5, 4 and 24h after APAP injection. 8-OHdG was significantly increased at 24h in the co-treatment group, but not with either catechol or APAP alone. Elevation of serum ALT and AST activities, decrease of reduced glutathione levels and histopathological liver changes were observed to the same extents in both APAP-treated groups. In view of the finding of positive hepatocytes for NO(2)Tyr prior to generation of 8-OHdG, the process of oxidative DNA damage might involve RNS formation. Precise quantitative analysis of NO(2)Tyr by means of liquid chromatography with tandem mass spectrometry (LC-MS/MS) in an additional study with the same experimental protocol confirmed increase of RNS due to the reaction of catechol with NO produced after APAP-induced hepatitis. The overall data imply that antioxidants with a catechol structure can cause oxidative DNA damage under inflammatory conditions.
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PMID:Dietary catechol causes increased oxidative DNA damage in the livers of mice treated with acetaminophen. 1957 46

Electrophoretic patterns of normal dog plasma in veronal buffer at pH 8.5 are shown to be essentially similar to patterns of human plasma. Dog albumin has a higher mobility than human albumin and in a mixture of dog and human plasmas migrates as a partially separated peak. Normal dog plasma frequently shows four alpha globulin peaks. Rates of restoration of plasma protein components in dogs subjected to acute plasmapheresis have been studied by electrophoresis. During the first 24 hours following such acute depletion, appreciable quantities of all electrophoretic components of the plasma proteins enter the circulating blood stream even when food is not given and has not been given for 12 hours before plasmapheresis. In such fasting periods albumin and total globulin appear in approximately the proportions present in normal plasma. Alpha and beta globulins continue relatively elevated during subsequent days in which caloric and protein intakes are adequate for weight and nitrogen gains. Initial albumin levels, however, are regained more slowly than those of total globulin. The relative proportions of the electrophoretic components of plasma proteins may be disturbed from normal following a single acute depletion for as long as 2 to 3 weeks after the total protein level has returned to normal. Abnormally high beta globulin and fibrinogen, but a low albumin, were found in a dog with an acute and chronic cholangitis and hepatitis. Similar elevation of gamma globulin was noted in a dog in which a hemolytic reaction occurred.
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PMID:PLASMA PROTEIN METABOLISM-ELECTROPHORETIC STUDIES : RESTORATION OF CIRCULATING PROTEINS FOLLOWING ACUTE DEPLETION BY PLASMAPHERESIS. 1987 73

It has been reported that an active aloe polysaccharide isolated from Aloe barbadensis Miller exerted various pharmacological effects, such as anti-inflammatory, wound healing, anti-hepatitis, anti-gastric ulcer, and anti-tumorigenicity in animals. Adverse health effects of aloe are of concern in humans. Therefore, this study was conducted to investigate a tolerable upper intake level (UL) of active aloe or a maximal allowable daily intake (ADImax) of active aloe based on 4-wk oral toxicity investigation in ICR mice. An active aloe was daily administered to male and female ICR mice for 4 wk at different dose levels (0, 120, 600, 3000, or 15,000 mg/kg body weight [bw]). All animals were sacrificed at the end of the experiment and changes of body weight, food consumption, organ weights, and hematological and biochemical parameters were recorded. In this study, no changes in clinical signs, urinalysis, or hematological or biochemical analysis were observed. In females, a dose-dependent quantitative decrease in albumin (ALB) levels was observed, but it was not significant, due to wide interindividual variations. A significant decrease in male kidney weight was observed from the 120-mg/kg to the 15,000-mg/kg bw treatment groups, and blood urea nitrogen (BUN) levels were also quantitatively lower. A dose-dependent reduction in the body weight of females was also observed, which might be related to less food consumption. Based on the reduced kidney weights in males, the lowest-observed-adverse-effect level (LOAEL) of an active aloe was estimated to be 120 mg/kg bw in male ICR mice, and the UL or ADImax was 0.4 mg/kg bw/d [(120 mg/kg bw/d)/(100 for safety factor) x (3 for modifying factor)], or 24 mg for a 60-kg adult (24 mg x 200 = 4.8 g of aloe gel/d/adult), assuming that consumers utilize active aloe for a month. Data showed that an active aloe did not induce any remarkable subacute toxic effects, but decreased male kidney weights, which requires further investigation.
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PMID:Estimation of tolerable upper intake level (UL) of active aloe. 2007 18

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are created in normal hepatocytes and are critical for normal physiologic processes, including oxidative respiration, growth, regeneration, apoptosis, and microsomal defense. When the levels of oxidation products exceed the capacity of normal antioxidant systems, oxidative stress occurs. This type of stress, in the form of ROS and RNS, can be damaging to all liver cells, including hepatocytes, Kupffer cells, stellate cells, and endothelial cells, through induction of inflammation, ischemia, fibrosis, necrosis, apoptosis, or through malignant transformation by damaging lipids, proteins, and/or DNA. In Part I of this review, we will discuss basic redox biology in the liver, including a review of ROS, RNS, and antioxidants, with a focus on nitric oxide as a common source of RNS. We will then review the evidence for oxidative stress as a mechanism of liver injury in hepatitis (alcoholic, viral, nonalcoholic). In Part II of this review, we will review oxidative stress in common pathophysiologic conditions, including ischemia/reperfusion injury, fibrosis, hepatocellular carcinoma, iron overload, Wilson's disease, sepsis, and acetaminophen overdose. Finally, biomarkers, proteomic, and antioxidant therapies will be discussed as areas for future therapeutic interventions.
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PMID:Nitric oxide and redox regulation in the liver: part II. Redox biology in pathologic hepatocytes and implications for intervention. 2040 Jan 12


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