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At least 19 recordsLinked to original sources
PubMed1997

Effect of chronic ethanol feeding on lipid peroxidation and protein oxidation in relation to liver pathology.

Liver lipid peroxidation, nonheme iron, antioxidants, and protein oxidation were investigated in experimental alcohol-induced liver disease in the rat. Wistar male rats were intragastrically and continuously infused for 4 weeks with a high-fat diet plus an ethanol or an isocaloric amount of dextrose, maintaining a high blood alcohol level (200-300 mg%). This model induced fatty liver, spotty necrosis, and focal inflammation. This pathology was associated with an enhanced lipid peroxidation and a decrease in the major antioxidant factors. Hepatic alpha-tocopherol and glutathione concentrations were significantly decreased in ethanol-fed rats. Glutathione peroxidase (GPx) was also decreased, whereas glutathione S-transferase (GST) was unaffected. The nonheme iron level was significantly decreased. Protein oxidation was assessed through three parameters: protein thiols, protein carbonyl groups, and the activity of glutamine synthetase (GS), a centrilobular enzyme particularly susceptible to free-radical-mediated damage. Ethanol-fed rats had decreased protein thiol concentrations and reduced GS activity, together with increased protein carbonyls. A significant correlation between GS activity and the pathological score was observed. This study confirms the ethanol-related increase in lipid peroxidation and shows that ethanol impairs the hepatic antioxidant potential. Furthermore, evidence of oxidative protein damage is given, including decreased activity of a key enzyme of ammonia metabolism. These protein disturbances may contribute to the pathogenesis of the observed liver damage.

Animals↗
PubMed2000

Pronounced hepatic free radical formation precedes pathological liver injury in ethanol-fed rats.

BACKGROUND: The role of free radicals in alcoholic liver injury remains uncertain. These experiments were conducted to measure radical formation in rats that were fed alcohol along with either fish oil or saturated fats, which cause different types of liver pathology. METHODS: Liquid diets containing alcohol or isocaloric dextrose were administered to rats by intragastric infusion for 2 weeks. Radical intermediates detected by spin trapping were measured in bile. RESULTS: In rats that were fed alcohol plus fish oil, biliary concentrations of trapped radicals, which most likely originated from lipids, were 6-fold higher than in controls that were fed fish oil plus dextrose. High rates of radical formation persisted 24 hr after alcohol withdrawal, when all alcohol had been metabolized. In contrast, diets containing alcohol and medium chain triglycerides did not stimulate lipid radical formation. CONCLUSIONS: High rates of lipid radical formation were observed only in rats that were fed alcohol in combination with a fish oil diet, and a persistent flux of radical formation continued after alcohol withdrawal. These radical phenomena precede serious liver pathology, which develops after longer periods of fish oil plus alcohol diets.

Animals↗
PubMed1989

Determination of tissue iron and ferritin in liver pathology comparison of histochemical and biochemical results.

Results are presented from the determination of tissue iron and ferritin in 15 pathological livers (6 with steatosis, 8 with fibrosis/cirrhosis and 1 with haemochromatosis). The histological assessment according to the Rowe system, after Perls' staining, was compared with the measurement of the iron content in liver homogenate by flameless atomic absorption spectrophotometry. The results of the flameless atomic absorption spectrophotometry were less accurate than in normal livers, but the method can still be considered reliable with satisfactory precision. As in normal livers, the range of chemically determined values in the histological staining grades was considerable and there was quite an overlap between consecutive grades. The chemical determination of liver iron content is to be preferred. The levels of ferritin protein and ferritin iron follow the same pattern as the total iron content.

Ferritins↗
PubMed1980

Fasciola hepatica: influence of thymus function on the liver pathology in mice.

Liver pathology during experimental Fasciola hepatica infection was compared in thymus-deficient (nu/nu) mice and in thymus-bearing (+/+) mice, (back ground strain to nu/nu mice) and thymus-reconstituted nu/nu mice. Thymus deficiency resulted in unrestricted liver damage during the migration of the parasite in the liver. In nu/nu mice the migratory tracks were infiltrated by very few eosinophils and mononuclear cells, haemorrhages and liver cell necroses were extensive. Portal area reaction and bile duct hyperplasia were depressed. Regeneration of liver tissue, parenchymal and periportal fibrosis and plasma cell proliferation were reduced. The possible causal mechanisms involved in fluke induced liver pathology are discussed. It is suggested that a thymus-dependent cellular reaction modulates the tissue damage produced by F. hepatica.

Animals↗
PubMed1976

[Corelations between thrombocyte count, clinical diagnosis, and liver pathology in chronic liver diseases].

In 1488 cases of chronic liver disease thrombocyte content of peripheral blood, clinical diagnosis and histologic findings of the liver biopsy were correlated. Ranging from fatty infiltration to fatty cirrhosis or from slightly active chronic hepatitis to active postnecrotic cirrhosis, according to the extent of the liver injury a significant decrease of thrombocyte-count was evaluated. In case of non-active liver disease and posthepatitic status a thrombocytopenia also could be found. Cirrhotic transformation or proliferation of the connective tissue mainly in the periportal fields and inflammatory activity showed a significant correlation to the frequency of a thrombocyte decrease. A pathogenetic relation is ascribed to an increased thrombocyte storage in the spleen depending on the extent of the liver injury and the alteration of the portal blood stream up to a portal hypertension. Our results indicate such correlations of liver injury, portal pressure and platelet-pooling to thrombocyte-count even if the causal dependency cannot be proved.

Adult↗
PubMed2004

Decreased proteasome activity is associated with increased severity of liver pathology and oxidative stress in experimental alcoholic liver disease.

BACKGROUND: Because of its role in degrading the bulk of intracellular proteins and eliminating damaged proteins, the proteasome is important in maintaining cell viability. Previously, we showed a 35-40% decrease in proteasome peptidase activity when ethanol was administered to rats by intragastric infusion. We hypothesized that this reduction was caused by ethanol-elicited oxidative stress, the degree of which varies depending on the method of ethanol administration. This study examined the relationship of proteasome activity and content with ethanol-induced oxidative stress and the degree of liver injury. METHODS: Rats were given ethanol or isocaloric dextrose-containing liquid diets by intragastric infusion for 1 month. The diets contained medium-chain triglycerides (MCT), palm oil (PO), corn oil (CO), or fish oil (FO) as the principal source of fat. RESULTS: Rats given ethanol and MCT exhibited no significant liver pathology, whereas cumulative pathology scores in ethanol-fed rats given PO, CO, or FO were 2.5, 5.4 and 7.0, respectively, indicating that ethanol and FO caused the greatest liver damage. The severity of liver pathology in the last three groups of animals correlated with levels of lipid peroxides and serum 8-isoprostanes. Alpha smooth muscle actin, an indicator of stellate cell activation, was increased relative to controls in the livers of all ethanol-fed rats except FO-fed animals, in which both control and ethanol-fed rats had similar levels of this protein. In livers of CO and FO ethanol-fed rats, proteasome chymotrypsin-like activity was decreased by 55-60%, but there was no quantitative alteration in 20S proteasome subunit content. In contrast, ethanol affected neither proteasome activity nor its content in MCT- and PO-treated animals. CONCLUSIONS: Our findings indicate that the severity of liver injury and ethanol-induced oxidative stress is associated with a reduction in proteasome catalysis.

Animals↗
PubMed1998

Increased lipid peroxidation and impaired antioxidant enzyme function is associated with pathological liver injury in experimental alcoholic liver disease in rats fed diets high in corn oil and fish oil.

Increased hepatic oxidative stress with ethanol administration is hypothesized to be caused either by enhanced pro-oxidant production or decreased levels of antioxidants or both. We used the intragastric feeding rat model to assess the relationship between hepatic antioxidant enzymes and pathological liver injury in animals fed different dietary fats. Male Wistar rats (5 per group) were fed ethanol with either medium-chain triglycerides (MCTE), palm oil (PE), corn oil (CE), or fish oil (FE). Control animals were fed isocaloric amounts of dextrose instead of ethanol with the same diets. The following were evaluated in each group: liver pathology, lipid peroxidation, manganese superoxide dismutase (MnSOD) levels, copper-zinc SOD (CuZnSOD) levels, glutathione peroxidase (GPX) levels, and catalase (CAT) levels. All enzymes were evaluated using activity assays and immunoblots. Rats fed FE showed the most severe pathology (fatty liver, necrosis, and inflammation), those fed CE showed moderate changes, those fed PE showed fatty liver only, and those fed MCTE were normal. Parameters indicative of lipid peroxidation (conjugated dienes and thiobarbituric acid-reactive substances) were also greater in rat livers from animals fed the diets high in polyunsaturated fatty acids (CE and FE). CuZnSOD, GPX, and CAT activities showed an inverse correlation (r=-.92, P < .01) with severity of pathological injury, with the lowest levels for both enzymes found in FE-fed rats. Decreased enzyme activity in CE- and FE-fed rats was accompanied by similar decreases in immunoreactive protein. Ethanol administration did not cause significant decreases in enzyme activity in groups that showed no necroinflammatory changes (MCTE and PE). MnSOD activity showed no significant change in any ethanol-fed group. Our results show that decreases in CuZnSOD, GPX, and CAT occur in rats showing pathological liver injury and also having the highest levels of lipid peroxidation. These results suggest that feeding dietary substrates that enhance lipid peroxidation can exacerbate both ethanol-induced oxidative damage as well as necroinflammatory changes. The decrease in activity of antioxidant enzymes observed in animals fed diets high in polyunsaturated fatty acids and ethanol could possibly increase the susceptibility to oxidative damage and further contribute to ethanol-induced liver injury.

Animals↗
PubMed2025

Serum N-glycomics for non-invasive detection of significant liver pathology across clinical phases of treatment-na&#xef;ve chronic hepatitis B.

BACKGROUND: Early identification of significant liver pathology is crucial for timely antiviral intervention in individuals with chronic hepatitis B (CHB) infection. Current non-invasive methods show limited accuracy in detecting occult liver damage, particularly in those with normal ALT. This study evaluated serum N-glycan profiles for diagnosing significant liver pathology in treatment-na&#xef;ve CHB patients across clinical phases. METHODS: This cross-sectional study analyzed 626 treatment-na&#xef;ve CHB patients confirmed by liver biopsy, classified according to 2025 EASL guidelines. Serum N-glycan profiles were determined using DNA sequencer-assisted fluorophore-assisted carbohydrate electrophoresis. Significant liver pathology was defined as inflammation grade&#x2009;&#x2265;&#x2009;G2 and/or fibrosis stage&#x2009;&#x2265;&#x2009;S2 (per Scheuer scoring system). Multivariate logistic regression models were developed and compared with traditional non-invasive markers. RESULTS: Among 626 CHB patients, 66.0% had significant inflammation and 58.9% had significant fibrosis. Patients with significant pathology showed characteristic alterations, with elevated P1, P3, P6, P7, P11 peaks and decreased P0, P5, P8, P10 peaks (all p&#x2009;<&#x2009;0.0001). Compared to respective infection phases, hepatitis phases showed P1 increases of 19.6% and 36% in HBeAg(+) and HBeAg(-) patients, with P11 increases of 82.4% and 73.4%, while P0 decreased by 20.3% and 27.6%, and P10 by 21.6% and 20.3%. Relative to mild pathology (G and S&#x2009;<&#x2009;2), P1 increased by 27% in significant pathology (G and/or S&#x2009;&#x2265;&#x2009;2), reaching 58.7%/48.7% in G4/S4 stages (vs. G0/S0). In ALT-normal HBeAg(+) infection phase, P1 increased by 80.2%/65.8% in G4/S4 stages (vs. G0/S0), with P2 also increasing by 54.1%/45.2%. Multivariate analysis identified P11 as strongest risk factor (OR&#x2009;=&#x2009;3.84, 95%CI: 1.74-8.45, p&#x2009;=&#x2009;0.0008), followed by P1 (OR&#x2009;=&#x2009;2.04, 95%CI: 1.57-2.64, p&#x2009;<&#x2009;0.0001) and P7 (OR&#x2009;=&#x2009;1.75, 95%CI: 1.31-2.34, p&#x2009;=&#x2009;0.0002), while P2 (OR&#x2009;=&#x2009;0.07, 95%CI: 0.02-0.26, p&#x2009;<&#x2009;0.0001) and P0 (OR&#x2009;=&#x2009;0.30, 95%CI: 0.12-0.79, p&#x2009;=&#x2009;0.0140) served as protective factors. The glycomics combined model (AUC&#x2009;=&#x2009;0.876 (0.844-0.908)) achieved superior performance and outperformed the clinical model (AUC&#x2009;=&#x2009;0.818 (0.779-0.857)), LSM (AUC&#x2009;=&#x2009;0.817 (0.775-0.858)), APRI (AUC&#x2009;=&#x2009;0.830 (0.792-0.867)), and FIB-4 (AUC&#x2009;=&#x2009;0.672 (0.621-0.723)) (all p&#x2009;<&#x2009;0.001), with 78.7% sensitivity and 83.2% specificity. The optimized model reached AUC&#x2009;=&#x2009;0.917 (0.891-0.942) with accuracy 84.2%, with 78.7% sensitivity and 94.6% specificity. Both glycomics-based models maintained diagnostic capability in ALT-normal patients particularly in HBeAg(+) infection. CONCLUSIONS: Serum N-glycomics demonstrates promising potential for non-invasive identification of significant liver pathology in treatment-na&#xef;ve CHB patients, providing an alternative approach for early treatment decisions, especially in ALT-normal patients with occult liver damage.

Humans↗
PubMed2005

[Macroscopic liver pathology in patients with dissociated cholestasis].

OBJECTIVE: To establish the prevalence of liver focal pathology in patients with increase of alkaline phosphatase and gamma-glutamil transpeptidase and normal bilirubin (dissociated cholestasis), and to analyze the related risk factors for such pathology. METHODS: All laboratory studies of patients admitted to an Internal Medicine Department were reviewed prospectively throughout a period of 9 months. For the purpose of detecting focal liver pathology imaging liver studies (echography and/or CT) were carried out in those in which biochemical analyses showed dissociated cholestasis. RESULTS: A dissociated cholestasis pattern was found in 81 patients. In 13 of them (16%) focal liver pathology was demonstrated. The majority of the lesions (10 of 13) were local or metastatic malignant neoplasms. Sex, alcohol consumption, presence of diabetes mellitus, tumor or hepatobiliar disease previously known, or abnormalities in liver physical examination were not risk factors. No liver pathology was found in patients with an alkaline phosphatase level higher than double of gamma-glutamil transpeptidase level (sensitivity: 100%; negative predictive value: 100%). Diagnosis of a non-hepatic malignant neoplasm at discharge was associated to a risk 12 times bigger for the presence of liver lesions (p < 0.01). CONCLUSIONS: It is uncommon to find focal liver pathology in patients with dissociated cholestasis. It is more common to discover focal liver pathology in patients with non-hepatic tumors and less probable when phosphatase alcaline: gamma-glutamil transpeptidase ratio is higher than two.

Adult↗
PubMed2004

[Surgical requirements for radiological diagnostics of liver pathologies].

BACKGROUND AND PURPOSE: Radiology is an essential preoperative tool for a liver surgeon to plan extent of resection and potential difficulties during liver surgery. MATERIAL AND METHODS: Primary goal in defining liver pathologies is a careful patients' history, a clinical evaluation and reviewing at least one radiological film one could acquire. Don't rely on written reports that may direct you in a useless track. This overview tries to address the essential radiological requests of a surgeon in defining liver tumors ethiology and best optional treatment. RESULTS: Major advances in radiologic diagnostics led to an improvement in the adequate staging of a given liver pathology. Therefore we are nowadays able to inform our patients about possible treatment options without leaving a big gap to possible intra-operative findings which may alter the therapy. Surgical exploration to define therapeutic strategies becomes fundamental only in a minority of patients with unclear preoperative imaging studies. DISCUSSION: Interdisciplinary groups should define future strategies in a patient with a given liver pathology. Specialisation has defined the hepatobiliary surgeon which should be consulted in case of a liver or biliary tumor to guide possible therapeutic treatment options.

Hepatectomy↗
PubMed1978

[HB-antigenemia and liver pathology].

The review deals with liver pathology in asymptomatic carriers of hepatitis B antigen. Information on the pattern and frequency of liver affection in carriers of HB antigen, on morphological methods for the detection of HB antigen in the liver tissue, on the frequency of the antigen detection in the liver tissue in asymptomatic antigen carriers and in liver diseases with HB antigenemia is presented. The data concerning the clinical and prognostic importance of hepatitis B antigen detection are given.

Hepatitis B Antigens↗
PubMed1983

[Fibroplastic reactions in liver pathology].

The connective tissue in liver biopsies from 880 patients with acute and chronic liver diseases was studied by means of the modern morphological methods--histochemistry, histoenzymology and electronmicroscopy. It was found that various forms of liver fibrosis (intralobular, portal and septal ones) accompany liver pathology with various frequency. They are of different value in the clinical manifestation and development, in diagnostics and prognostic estimates in each case.

Adult↗
PubMed1996

[Role of hepatotropic viruses in liver pathology in Southwestern Cameroon].

Between 1990 and 1992 (2 years), 102 patients with clinical liver pathology underwent standardized clinical, pathological, sonographic and serologic investigations (HAV, HBV, HCV, HDV autoantibodies and tumor markers). During the same period seroepidemiological studies with the same parameters as above were performed on the following control groups: healthy pregnant women (n = 383), blood donors (n = 85), HIV-positive individuals (n = 93), and hospitalized patients in all age groups with minor ailments unrelated to liver pathology (n = 108). The results are discussed in detail. Virtually all adults had HAV infection. HBV and HCV infection appears to play a major role in chronic liver pathology in southern Cameroon. The two infections frequently occur together (over 40% of liver cases) and correlate significantly with liver cirrhosis. The marked prevalence of HBV and HCV markers in healthy pregnant women is of epidemiological concern due to the potential for vertical transmission of the infection (immunization). Endemic infections such as falciparum malaria are probably responsible for unspecific stimulation of the immune system, which is reflected in a generally marked prevalence of autoimmune markers in liver patients and controls, since histologically there was no evidence of autoimmune liver disease.

Abdomen↗
PubMed1994

Changes in cytochromes P-450, 2E1, 2B1, and 4A, and phospholipases A and C in the intragastric feeding rat model for alcoholic liver disease: relationship to dietary fats and pathologic liver injury.

The influence of dietary fat and alcohol on hepatic microsomal levels of cytochromes P-450 2E1, 2B, and 4A; phospholipases A and C; and UDP-glucuronosyltransferase was studied in the intragastric feeding rat model for alcoholic liver injury. Eight groups of animals were evaluated. Control and ethanol fed rats received either saturated fat or corn oil and were killed after 2 weeks and 1 month of feeding. All animals were pair-fed by continuous infusion of liquid diet through permanently implanted gastric cannulas. Alcoholic liver injury developed only in the corn oil-ethanol-fed groups and was manifest by 1 month. Livers were subjected to the following analyses: pathologic evaluation of liver injury; levels of cytochromes P-450 2E1, 2B, and 4A protein and mRNA; aniline hydroxylase activity; and phospholipase A and C and UDP-glucuronosyltransferase activities. Ethanol-induced increases in cytochromes P-450 2E1 and 2B protein determined by Western blotting were greatest in the corn oil-ethanol-fed group, which developed pathologic changes in the liver. Cytochromes P-450 2E1 and 2B1 mRNA levels were unaffected, suggesting that posttranscriptional mechanisms are responsible for the increase in the corresponding P-450 proteins. In contrast, cytochrome P-450 4A levels were higher in the saturated fat-ethanol groups compared with the corn oil-ethanol groups. Phospholipase A and phospholipase C levels were higher in the corn oil-ethanol groups compared with pair-fed dextrose controls and the saturated fat-ethanol groups. UDP-glucuronosyltransferase levels declined with time in the ethanol-fed groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

[Assessment of liver pathology on the basis of biochemical and ultrasonographic findings in a group of alcohol dependent patients].

The paper presents the assessment of liver pathology based on clinical examinations, biochemical findings and abdominal ultrasound examination with colour Doppler modalities in a group of 40 alcohol dependent patients. Special regard was paid to the liver, it is size, echogenecity, homogeneity and flow patterns in the portal vein. No significant correlations between the biochemical and USG parameters of liver pathology and the intensity of alcohol withdrawal and the level of the alcohol dependence syndrome were found. It can be concluded that the biochemical parameters as well as ultra sound diagnosis of alcoholic liver disease do not allow to make a final diagnosis of liver pathology.

Adult↗
PubMedDate not supplied

Ultrastructural liver pathology in patients with minimal liver disease and alpha 1-antitrypsin deficiency: a comparison between heterozygous and homozygous patients.

A light and electron microscopic investigation of liver tissue from three homozygous (Pi-type ZZ) and three heterozygous (Pi-type MZ) alpha 1-antitrypsin deficiency patients is presented. All had slightly elevated levels of serum amino transferases as the only signs of liver damage. Light microscopical investigation showed minor periportal fibrosis and periodic acid-Schiff-positive globules in the homozygous patients, but no specific findings besides fatty changes were seen in the heterozygous patients. Electron microscopical investigation was performed on periportal and centrilobular areas separately. In the three homozygous patients, dilatation of endoplasmic reticulum was found in many periportal liver parenchymal cells. In these cells, a marked increase in peroxisomes was also noted and in some instances they showed signs of cell necrosis. Evidence of Kupffer cell heterophagy of such cells was also found, thus indicating that they had died. Only in one liver parenchymal cell from one of the three heterozygous patients was evidence of a dilated endoplasmic reticulum found. No increase in peroxisomes was found and no apparent signs of liver cell necrosis were noted. An increased amount of lipofuscin-like material in the lysosomes was encountered in liver cells both from patients with homozygous and heterozygous alpha 1-antitrypsin deficiency. Based on these findings, it is suggested that cell death occurs in cells with a dilatation of the endoplasmic reticulum. If these findings are important for the pathogenesis in liver disease in alpha 1-antitrypsin deficiency, the present study suggests that the risk to develop liver disease is less in heterozygous patients since, with one exception, alterations of the same nature were not found in their hepatocytes.

Adult↗