Chronic Toxic Hepatitis Research Articles

Morphological and functional state of liver of sex matured females of white rats in the conditions of experimental toxic hepatitis

<p>Parafunctions of organs of the reproductive system occupy one of the main places among gynaecological diseases<br />and are the issue of the day, because they result not only in the loss of capacity but also decline of reproductive function.<br />Concomitant diseases play a considerable role in the development of this pathology. Women of reproductive age<br />often have combination of violations of menstrual function with chronic hepatitis of different genesis. With the aim of<br />the detailed study and analysis of the indicated problem an experimental study was undertaken. We made a model<br />of chronic toxic hepatitis for the sex matured females of white rats. There were studied the results of morphological<br />changes in the liver of experimental animals, state of enzymatic, protein-synthesizing liver functions in the conditions<br />of experimental toxic hepatitis and their correlation with the results of clinical and biochemical researches. 50 sex<br />matured females of white rats were examined whom chronic toxic hepatitis (CT H) was modelled.</p>

Features of reparative regeneration of the liver tissue in rats during experimental tetrachloromethanic and alcoholic hepatitis

Chronic hepatitises are common pathology of the liver, which often end with the formation of cirrhosis (LC). Aim. The features of reparative regeneration of liver tissue, as well as pathomorphosis of chronic toxic hepatitis of different etiology, namely tetrachloromethanic (CTH) and alcoholic (CAH), were studied in the experiment in immature rats. Methods and results. The results of flow cytometric and morphological studies have shown that in rats with CTH significant impairment of lymph flow develops in the form of edema in liver tissue; the number of functioning lymphatic vessels with the presence of lymphangiectasias increases that can significantly influence the processes of fibrogenesis. In rats with CAH fatty liver combined with hydropic one is observed. It was established that a characteristic feature of hepatocytes population of immature rats in CTH is increase of nuclear DNA ploidy>8c, reducing of the percentage of nuclei in the range G 0 G 1 with increasing percentage of cell nuclei in the S-phase, nuclear DNA fragmentation and proliferation index. In CAH, unlike CTH, there was a decrease of synthetic processes in the nuclei of hepatocytes, and polyploidy of nuclear DNA was not observed. Conclusion. This demonstrates the antiproliferative effect of ethanol.

Особливості продукції трансформувального фактора росту β1 у щурів в умовах хронічного токсичного гепатиту

Особливості продукції трансформувального фактора росту β1 у щурів в умовах хронічного токсичного гепатиту

Triggering ubiquitination of IFNAR 1 protects tissues from inflammatory injury

Type 1 interferons (IFN) protect the host against viruses by engaging a cognate receptor (consisting of IFNAR1/IFNAR2 chains) and inducing downstream signaling and gene expression. However, inflammatory stimuli can trigger IFNAR1 ubiquitination and downregulation thereby attenuating IFN effects in vitro. The significance of this paradoxical regulation is unknown. Presented here results demonstrate that inability to stimulate IFNAR1 ubiquitination in the Ifnar1SA knock-in mice renders them highly susceptible to numerous inflammatory syndromes including acute and chronic pancreatitis, and autoimmune and toxic hepatitis. Ifnar1SA mice (or their bone marrow-receiving wild type animals) display persistent immune infiltration of inflamed tissues, extensive damage and gravely inadequate tissue regeneration. Pharmacologic stimulation of IFNAR1 ubiquitination is protective against from toxic hepatitis and fulminant generalized inflammation in wild type but not Ifnar1SA mice. These results suggest that endogenous mechanisms that trigger IFNAR1 ubiquitination for limiting the inflammation-induced tissue damage can be purposely mimicked for therapeutic benefits.Subject Categories Immunology; Digestive System

Contribution of Maternal Chronic Experimental Hepatic Disease to the Development of Nonspecific Cell Resistance in the Progeny

Morphofunctional pecularities of the bone marrow neutrophil maturation were studied in the progeny of female rats with chronic experimental toxic hepatitis, similar to hepatitis B by morphological, biochemical, and physiological characteristics. The lysosomal, phagocytic, and killing activities of cells were reduced during the morphologically identifiable stages of neutrophilopoiesis (myeloblasts, promyelocytes, myelocytes, metamyelocytes, stab and segmented neutrophils).

Mechanisms of Hepatoprotective Effect of Immobilized Granulocyte colony-Stimulating Factor

The effect of immobilized granulocyte CSF on morphological characteristics and functional state of the liver was studied during chronic toxic hepatitis. The mechanisms of the therapeutic action of this agent were evaluated. The product had a strong hepatoprotective effect and exhibited the antiinflammatory and antisclerotic properties. The mechanism of activation of reserve systems for cell renewal (involved in restoration of the liver tissue) is probably related to an increase in proliferative activity of early precursor cells in the bone marrow, mobilization of these cells into the peripheral circulation, and directed homing into the liver tissue where they activate local regenerative mechanisms and prevent hepatocyte destruction. It should be emphasized that the concentration of SDF-1 increases in the liver tissue, but decreases in the bone marrow. These changes create the concentration gradient, which determines the migration of undifferentiated precursor cells to the liver.

Activity of Sphingomyelinase in Rat Liver in Acute and Chronic Toxic Hepatitis: Proportion between Peroxidative and Phospholipase Pathways of Lipid Bilayer Modification

We showed that sphingomyelinase activity in the liver increased only during the acute phase of toxic hepatitis. Peroxidative modification of hepatocyte membrane bilayer prevailed during the acute phase, while after transformation of the process to the chronic phase phospholipase pathway predominated.

Functional Activity of Sphingomyelin Cycle in Rat Liver in Chronic Toxic Hepatitis

Activities of sphingomyelinase and ceramidase decreased in the liver in chronic toxic hepatitis and the balance between the levels of proapoptotic ceramide and antiapoptotic sphyngosine-1-phosphate shifts towards the latter substance. Pronounced changes in the qualitative and quantitative composition of fatty acids in the sphingomyelin cycle effector molecules were revealed.

Pro- and Antioxidants in the Central Lymph in Experimental Chronic Toxic Hepatitis

Using rat model of chronic toxic hepatitis we showed the involvement of the lymph system in the formation of the response to toxic liver damage consisting in deposition of LPO products in the central lymph and active involvement of antioxidants in their neutralization with redistribution of ceruloplasmin into lymph vessels against the background of reduced a-tocopherol content in the central lymph.

Fumonisin B1-induced hepatocellular and cholangiocellular tumors in male Fischer 344 rats: potentiating effects of 2-acetylaminofluorene on oval cell proliferation and neoplastic development in a discontinued feeding study.

Fumonisin B1 (FB1) is a naturally occurring mycotoxin produced by Fusarium verticillioides. Dietary exposure to FB1 has been linked to human cancer in certain parts of the world, and treatment with FB1 causes oval cell proliferation and liver tumors in rats. To study the potential role of oval (liver progenitor) cells in the cellular pathogenesis of FB1-induced liver tumors, we gave male F344 rats prolonged treatment with FB1 for 25 weeks, followed by return to control diet until 50 weeks ('stop study'). The time course of FB1-induced liver lesions was followed by examination of serial liver biopsies at set time intervals and post-mortem liver tissue at the end of the study. The effects of different FB1 treatment regimens (5 versus 25 weeks), as well as the modulating effect of 2-acetylaminofluorene (2-AAF), on the kinetics of oval cell proliferation and development of liver tumors were compared. Prolonged treatment with FB1 in normal diet caused persistent oval cell proliferation and generation of both hepatic adenomas and cholangiofibromas (CFs). These liver lesions occurred in the setting of chronic toxic hepatitis and liver fibrosis/cirrhosis, similar to that seen in human hepatocarcinogenesis. Some adenomas and CFs were dysplastic, and one post-mortem liver contained a hepatocellular carcinoma. OV-6+ oval cells were noted in close relation to proliferative neoplastic liver lesions, and some of these lesions expressed OV-6, suggesting that all these cell types were derived from a common progenitor cell. 2-AAF enhanced the size of FB1-induced glutathione S-transferase pi+ hepatocellular lesions and the incidence of CFs in post-mortem liver specimens, but this was not statistically significant. In conclusion, this study supports the involvement of dietary FB1 in liver carcinogenesis in male F344 rats. Oval cells may be the source of both the hepatocellular and cholangiocellular tumors induced by prolonged treatment with FB1. 2-AAF appears to have an enhancing effect on FB1-induced liver tumors, presumably due to its potent inhibitory effects on hepatocyte regeneration.

Effects of homeopathic preparations on the liver in rats with acute and chronic toxic hepatitis.

Ultralow doses of antibodies to phenobarbital and their mixture (1:1) with ultralow doses of antibodies to cholecystokinin reduced the severity of structural and metabolic disturbances in the liver of rats with acute CCl4-induced hepatitis. The mixture of antibodies had no effect on the course of CCl4-induced hepatitis.

Hepatoprotective properties of potentiated antibodies to cholecystokinin.

Ultralow doses of antibodies to cholecystokinin prevented hepatocyte death, delayed the formation of the connective tissue, and normalized plasma of liver enzyme in rats with experimental acute and chronic toxic hepatitis.

Hepatoprotective properties of aqueous extract from Pentaphylloides fruticosa during chronic toxic hepatitis.

Hepatoprotective properties of Pentaphylloides fruticosa L. aqueous extract were studied using rat model of chronic toxic hepatitis. The preparation normalized alanine aminotransferase activity and bilirubin concentration in the plasma. Aqueous extract of Pentaphylloides fruticosa produced a protective effect on microsomal metabolism of xenobiotics and lipid peroxidation activity in the plasma and microsomal liver fraction.

Hepatoprotective properties of soybean proteins and their use for dietary therapy of chronic toxic hepatitis

Hepatoprotective effect of a diet containing soybean proteins most pronounced in soybean milk was demonstrated on the model of chronic toxic hepatitis. Results of biochemical studies correlate with morphological data indicating that soybean proteins hold much promise for supportive therapy of patients with chronic liver diseases.

Effect of ozone on the liver in experimental chronic hepatitis

Short-term administration of ozonized physiological solution to rats with chronic toxic hepatitis reduces the content of total lipids in the liver tissue, activates antioxidant enzymes, normalizes the level of diene conjugates, and reliably increases adenosine nucleotides, the number of normal hepatocytes being increased 2.2-fold. The data suggest that ozone can be used as a stimulator of regeneration of the pathologically altered liver.

The histopathology of the liver in older patients with hepatitis B virus surface antigenaemia

The histopathology of the liver and the detectability of intrahepatic hepatitis B virus (HBV) markers were studied in 34 autopsy cases in elderly patients (mean age 73.9 years, range 60-91 years) who had had a history of positive HBV surface antigenaemia prior to death. Seven of 14 persistent HBV carrier cases (group A) in which long-lasting HBV surface antigen (HBsAg) carriage in the sera had been confirmed by sequential assays, and 5 out of 15 HBV-infected people (group C, single assay) showed significant primary liver damages including chronic hepatitis, toxic hepatitis, liver cirrhosis and hepatocellular carcinoma. In 5 cases (group B), one of which was type B liver cirrhosis, HBsAg became negative and HBsAb appeared during the follow-up period (up to 33 months). Among confirmed HBV carriers, HBsAg and HBV core antigen were most frequently found in the liver of cirrhotic cases with and without hepatocellular carcinoma (5 of 6), whereas these were rarely detected in those with non-specific changes or slight hepatitic activity (1 of 7). All 5 cases in group B were negative for histological HBV-related antigens and the findings in group C were variously interpreted. Post-mortem cases of the aged HBV carriers who survived their mean life expectancy represent an important population in which to study the natural history of HBV carriers.

Hepatitis in vervet monkeys caused by Fusarium moniliforme

The fungus Fusarium moniliforme Sheldon is a common contaminant of maize ( Zea mays L.) intended for human and animal consumption throughout the world. Culture material of F. moniliforme MRC 826, isolated from home-grown maize in an area in Transkei, southern Africa, with a high rate of human oesophageal cancer, was highly toxic to vervet monkeys ( Cercopithecus pygerythrus). Ten monkeys were fed a standard primate diet which contained various amounts of culture material for 180 days. Two control monkeys received the standard diet without culture material. Pathological changes observed in liver biopsies taken by laparotomy were characterized by focal disturbance of the trabecular structure, degeneration and necrosis of hepatocytes, mononuclear infiltration, and in severe cases by cirrhosis. Biochemical changes, particularly increases in liver enzyme activities in serum, paralleled the liver damage seen by light microscopy. The acute, subacute and chronic toxic hepatitis induced in various degrees in all the monkeys fed fungal culture material showed close similarity with human viral hepatitis. The lesions also have some similarities to those induced in primates by aflatoxin, but differ in several respects. Ultrastructural nuclear and nucleolar changes caused by F. moniliforme, i.e. marginal clumping of chromatin and large nucleoli with segregation of fibrillar and granular components, suggested some similarity with the changes reported to be caused by aflatoxin and some other hepatocarcinogens. A long-term feeding experiment in vervet monkeys with F. moniliforme MRC 826 and attempts to isolate and chemically characterise the hepatotoxic metabolite(s) produced by this fungus are being continued.

Odontes serotina as a stimulator of regeneration processes in rat liver in chronic toxic hepatitis

Odontes serotina as a stimulator of regeneration processes in rat liver in chronic toxic hepatitis

Thirteen-week toxicology studies of 1-amino-2,4-dibromoanthraquinone in Fischer [formula omitted] rats and B6C3F 1 mice

1-Amino-2,4-dibromoanthraquinone (ADBAQ), an intermediate in the production of commercial dyes for wool, silk, and synthetic fibers, was selected for toxicology and carcinogenesis studies in two rodent species. In advance of the 2-year studies, 13-week studies were conducted in male and female F344 N rats and B6C3F 1 mice which were fed a diet containing ADBAQ at concentrations of 0, 0.25, 0.50, 1.00, 2.50, and 5.00%. ADBAQ stained the skin and fur red at all doses in rats and at 1.00% and higher concentrations in mice. Lethargy and emaciation were noted at the 2.50% and higher doses in rats of both sexes. In general, the absolute weight of the liver and the liver/organ weight ratios increased in both sexes and species at all doses. Treated rats developed a chronic toxic hepatitis characterized by hepatocytomegaly, centrilobular vacuolar degeneration and necrosis, regenerative nodules, acute necrotizing cholangitis, bile duct hyperplasia, chronic active inflammation in periportal areas, and focal pigmentation. The hepatopathy occurred at all doses in males and at 0.50% and higher in females and correlated with elevations of serum glutamic-pyruvic and glutamic-oxaloacetic transaminases, leukocytosis, and neutrophilia. Hyaline droplet degeneration in the proximal convoluted tubules of the kidneys occurred in male rats, and uterine atrophy was observed in female rats at 1.00% and higher. Anemia occurred in both sexes of rats at all doses and thymic atrophy was observed in both sexes of high-dose rats. In male mice minimal dose-related lesions in the liver included centrilobular glycogen depletion at 1.00% and higher and pigmentation at all doses. At comparable doses, ADBAQ was considered to be markedly toxic in rats and of minimal nonlife-threatening toxicity in mice.

Safety and health in boatbuilding and repair.

Boatbuilding is a complex, chemically intensive industry which employs approximately 43,000 workers in the United States, 77% of them in shops with fewer than 20 workers. Boatbuilders and repairers are at high risk of occupational injury from falls, lacerations, low back trauma, repetitive motion, noise, burns, fires, and explosions. Also they are at risk of acute and chronic illness, including dermatitis, toxic hepatitis, peripheral neuropathy, and chronic encephalopathy as a result of their occupational exposures to such materials as styrene, resins, solvents, paints, welding fumes, and coating systems. Boatbuilders also are exposed to toxic woods and to lead. Hazard recognition is the first step toward reduction of injury and disease in boat building. Control of recognized hazards is achieved through engineering controls, ventilation in particular, and through medical surveillance. Strong programs for injury prevention and for health and safety education will produce significant health and economic benefit in the boatbuilding industry.