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At least 19 recordsLinked to original sources
PubMed1987

Biochemical effects of acute stress on energy metabolism in liver damaged rats.

Rats having a non-necrotic damaged liver or a necrotic damaged liver produced by D-galactosamine administration were restrained in water for 0.5, 1, 2, 4, 6, 8 and 12 hours. Serial changes in intrahepatic energy metabolism were compared with those in normal liver. Energy charge, which represents the degree of equilibrium between the energy producing and consuming systems, and cyclic AMP, an intracellular messenger mediating the action of hormones, showed biphasic increases before and after 2 hr in the damaged livers. The lactate/pyruvate ratio, which reflects the cytosolic redox state, markedly increased at 0.5 hr in the damaged livers but returned to the pre-stress level after 1 hr in the non-necrotic damaged liver and after 4 hr in the necrotic damaged liver, showing a transient reduced state. The beta-hydroxybutyrate/acetoacetate ratio, which represents the mitochondrial redox state, decreased at 0.5 hr and returned to the pre-stress level at 1 hr in the non-necrotic damaged liver, exhibiting a transient oxidized state. However, in the necrotic damaged liver, the value decreased at 0.5 hr remained low thereafter, demonstrating a persistent oxidized state. These findings show that, in severely damaged liver, stress has more marked effects on hepatic energy metabolism.

Acetyl Coenzyme A↗
PubMed1991

Relationship of liver damage and liver regeneration after carbon tetrachloride treatment in rats.

Various doses of carbon tetrachloride (0.625 mmol to 10 mmol CCl4/kg body weight) were administered to female Wistar rats. Liver damage after a single treatment was evaluated by serum aminotransferase levels and by the extent of necrotic areas in parenchyma. Liver regeneration was evaluated by 3H-thymidine incorporation into liver DNA and by the number of dividing hepatocytes. Mitotic index of hepatocytes rose in parallel with the specific activity of DNA and with the extent of necrosis. However, the activities of serum aminotransferase AST and ALT increased much more rapidly and did not correlate either with necrosis or with regeneration rate. Increased membrane permeability in morphologically intact cells, increased synthesis of the enzymes by the liver as well as the leakage from necrotic cells are discussed as possible causes of the high aminotransferase activities in serum.

Alanine Transaminase↗
PubMed1979

Alcohol-induced brain damage and liver damage in young males.

37 alcoholic males under the age of 35 were examined clinically, by psychometric tests, by computerised tomography (CT scans), and by liver biopsy. Factors other than alcoholism that might have caused brain damage were excluded. The prevalence of brain damage in this group was far greater than that of severe liver damage: 59% were intellectually impaired and 49% had cerebral atrophy on CT scan, whereas only 19% had cirrhosis. There was no significant correlations between the degree of liver damage and the degree of intellectual impairment (p greater than 0-05), nor between the degree of intellectual impairment and the presence of cerebral atrophy. The CT scan is an inadequate measure of functional brain damage, psychometric testing is preferable. Other neurological complications of alcoholism were not impressive. Disabling intellectual impairment may be the earliest complication of chronic alcoholism and may arise early in the alcoholic career.

Adult↗
PubMed1979

Liver damage after liver hilus dearterialization in dogs.

Twenty-one harrier dogs underwent a standardized liver hilus dearterialization with (7) or without (14) cholecystectomy using six sham-operated dogs as controls. Seven dogs died, only one of which was in the dearterialization and cholecystectomy group. S-OCT and s-GDH were increased at 90 minutes after dearterialization. There was no statistical difference between the groups at 90 minutes. On the first day after dearterialization, the activity of s-OCT, s-GDH, s-ALAT rose significantly (p less than 0.005). The activity of s-ASAT was, however, increased to the same extent both in the dearterialized and the sham-operated animals. A normalization of the serum enzyme activities was usually seen after one week. S-ALP increased on the first day (p less than 0.005) and still higher values were noted on the seventh day after dearterialization. Cholecystectomy did not affect any of these results except mortality. Liver oxygen consumption, in vitro was unchanged throughout the experiment. The oxygen consumption of bile duct mucosal scrapings one week after dearterialization was similar to the corresponding values in the controls. The results indicate that the dearterialization leads to a definite but mild and reversible mitochondrial and cell membrane damage. The results indicate further the need of adequate controls when the effects of dearterialization on the liver are studied.

Alanine Transaminase↗
PubMed1979

[Effect of thiol compounds on experimental liver damage (I). Preventive effect of tiopronin (2-mercaptopropionylglycine) on liver damage induced by carbon tetrachloride (author's transl)].

Effects of oral administration of tiopronin (2-mercaptopropionylglycine) on acute liver damage induced in rats by intraperitoneal administration of carbon tetrachloride (CCl4) were investigated. Tiopronin suppressed increase in serum transaminase activity, accumulation of liver triglyceride and decrease of liver glucose-6-phosphatase activity induced by CCl4. CCl4 induced a significant decrease of nonprotein thiol (NPSH) in the liver 24 hr after administration, but this decrease did not result in an increase of nonprotein disulfide in the liver. Tiopronin suppressed the decrease in NPSH induced by CCl4, but did not influence NPSH in normal rats 24 hr after administration. In addition to these biochemical findings, it was also noted that tiopronin prevented necrosis and decrease of glycogen in liver, as determined histologically. Other compounds such as cystamine, cysteine and glutathione proved to have a preventive effect on CCl4-induced liver damage as in the case of tiopronin. It was revealed that such preventive effect correlated to some extent with NPSH content in liver as well as serum transaminase activity and histological findings.

Alanine Transaminase↗
PubMed1979

[Effects of thiol compounds on experimental liver damage (II). Preventive and therapeutic effects of tiopronin (2-mercaptopropionylglycine) and glutathione on ethionine induced liver damage (author's transl)].

Preventive and therapeutic effects of tiopronin (2-mercaptopropionylglycine) and glutathione on ethionine induced liver damage were studied. Administration of 1 g/kg ethionine resulted in significant differences in the degree of liver damage, and such was dependent on the feeding conditions of the animals. The present experiment was performed under the conditions where the most serious liver damage was observed. In the experiment on the preventive effects, serum GOT and GPT were markedly elevated by ethionine, but such elevation could be suppressed by administering tiopronin or glutathione 10 min before ethionine administration. Liver nonprotein thiol (NPSH) content decreased by 40--60% of the normal level 16 hr after ethionine adminstration, but increased by 30--45% 24 hr later. Administration of tiopronin suppressed the initial fall of liver NPSH content caused by ethionine, but this tendency was not observed in the glutathione treatment. Both liver cholesterol and triglyceride increased in the ethionine treated rats, and triglycerides in particular decreased with administration of tiopronin or glutathione. In the experiment on the therapeutic effects, the maximal values of serum GOT and GPT brought by ethionine were suppressed by the thiol compounds given 16 hr after ethionine administration, but liver NPSH content and liver lipids were not influenced. Thus, tiopronin and glutathione are considered to have preventive and therapeutic effects on liver damage induced by ethionine.

Amino Acids, Sulfur↗
PubMed1976

Elimination of vasopressin by the normal and the damaged liver. Experiments on unanaesthetized normal and thiocetamide treated rats with a note on the influence of ethanol.

Arginine vasopressin was infused into the V. portae and into the V. cava of unanesthetized rats in water diuresis. The differential antidiuretic response of the same animal to these infusions was used to calculate extraction fraction of ADH by the liver. In the normal rat no extraction was detected. The liver of rats hydrated with 5% ethanol extracted 10% and that of rats treated with thioacetamide extracted 60% of the ADH infused into the portal vein. It is postulated that disturbances of liver cell function by narcotics and substances causing liver damage may liberate ADH-destroying ferments into the blood.

Acetamides↗
PubMed1974

Comparison of antigenicity of hepatoma cells, normal liver cells, foetal liver cells and chemically damaged liver cells in guinea-pigs immunized with hepatomata using the macrophage migration inhibition test.

The macrophage migration inhibition test has been used to study the immune responses of guinea-pigs immunized with injections of whole cells of both an allogeneic and a syngeneic hepatoma grown as established cell lines in tissue culture.A clear dose-response relationship between tumour cell concentration and migration inhibition was seen in immunized animals and no significant migration inhibition was seen in control animals. There was no cross reaction between the two tumours used. There was no cross reaction between whole isolated normal liver cells and tumour cells, or between foetal liver cells and tumour cells. Whole isolated liver cells from carbon tetrachloride damaged livers caused some degree of migration inhibition in both normal and immunized guinea-pigs but, taking this into account, they did not appear to cross react with hepatoma cells.

Animals↗
PubMed1975

Influence of phospholipids on liver damage. II. Changes in lipid content and synthesis after liver damage with carbontetrachloride and other agents.

Content and synthesis of lipids were studied in rats after carbontetrachloride poisoning and different treatments with phospholipids (EPL), as well as in some other conditions under which an increase in lipids occurs. The increase in neutral lipids during CCl4 poisoning is significantly reduced by pretreatment and--somewhat less--by posttreatment with EPL. Incorporation of acetate into triglycerides, phospholipids and cholesterol increases in CCl4 poisoning and this was not affected by EPL. Moreover, treatment with EPL had but little effect on the lipid accumulation induced by orotic acid feeding and partial hepatectomy. EPL promoted, however, slightly DNA synthesis after partial hepatectomy and protected DNA in thymus after whole body X-irradiation.

Acetates↗
PubMed1975

Liver damage after paracetamol overdose. Comparison of liver-function tests, fasting serum bile acids, and liver histology.

54 patients have been studied after paracetamol (acetaminophen) overdose. Liver-function tests and fasting serum bile-acids were measured daily; liver biopsy was done in all cases, and slides were examined "blind" to assess liver damage. The plasma-paracetamol was measured on one occasion. A histological abnormality was present in the livers of 53 of the 54 patients, and was minor in 23, moderate in 16, and severe in 14. In 6 patients with moderate and 18 with mild histological abnormality liver-function tests were normal. A serum-aspartate-aminotransferase above 400 units/1 was always associated with severe histological liver damage. Fasting serum bile-acids were raised in 51 of the patients with abnormal liver histology; the serum-bile-acid seemed to be a more sensitive indicator of mild liver-cell damage than was the transaminase level. There was, however, little correlation between increase in bile-acid concentration and the degree of histological abnormality. As a result of these investigations empirically determined levels of plasma-paracetamol have been drawn which give a guide to the likelihood of liver damage after paracetamol overdose.

Acetaminophen↗
PubMed1988

Relation between renal and hepatic excretion of drugs: VII. Hepatic and renal excretion of phenol red in thioacetamide-induced acute and chronic liver damage.

Acute and chronic liver damage was induced in rats by thioacetamide (TAA). Centrilobular liver cell damage associated with an accumulation of lipid droplets was produced by a single high dose (10 mg TAA/100 g b.m.). Liver fibrosis, micronodular and macronodular liver cirrhosis were induced by chronic TAA treatment (300 ml/l drinking water for 1.5, 3 or 6 months). Acute administration of TAA caused a significant decrease of hepatic phenol red excretion but no compensatory increase of its urinary excretion. In contrast, 24 h after bile duct ligation renal excretion of the dye increased by about 50%. After chronic exposure to TAA for three months hepatic phenol red excretion remained reduced and renal excretion raised significantly. This compensatory increase of urinary excreted phenol red amounts did not occur after 6 months of TAA treatment, probably as a result of additional nephrotoxicity of TAA. Two weeks after cessation of TAA exposure for 3 months, hepatic and renal phenol red excretion returned to normal. Bile flow per animal increased significantly after 3 months of TAA exposure. Apparently this is due to a reduced intrahepatic reabsorption of canalicular bile in TAA-damaged liver.

Animals↗
PubMed1990

Effect of aspartate and glutamate on carbon tetrachloride induced liver damage in rats.

Liver necrosis was produced in rats by administering 3 doses of a mixture of carbon tetrachloride + olive oil, 2 ml/kg, ip. The liver damage was evidenced by the elevated levels of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and gamma glutamyl transpeptidase (gamma-GT) and by histopathological observations of liver sections. Aspartate and glutamate administration (100 mg/kg, ip) significantly reduced these elevated levels of AST, ALT, and gamma-GT. Carbon tetrachloride induced liver necrosis was also found to be significantly reduced in aspartate and glutamate pretreated animals as observed macroscopically and histologically.

Animals↗
PubMed1992

Effect of adenosine and inosine on carbon tetrachloride-induced liver damage in rats.

Liver damage induced in rats by carbon tetrachloride (CCL4) was obvious macroscopically as well as microscopically in stained sections. Levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and gamma glutamyl transpeptidase (gamma-GT) were also significantly raised. Adenosine and inosine effectively countered the damage when these were given before and during the period during which CCl4 produces the typical damage. The beneficial effect was seen in biochemical as well as pathological studies.

Adenosine↗