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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of carbon tetrachloride (CCl4) and methylene chloride (MC) on the hepatic microtubular system and its relationship to the development of fatty liver were examined. Hepatic microtubule content was assessed using a specific colchicine-binding assay. These studies demonstrated that these 2 chlorinated methanes had no early effect on hepatic microtubule content. A significant decrease in microtubules was not observed until after the development of the fatty liver. In vitro tubulin polymerization studies demonstrated that neither CCl4 nor MC had a significant effect on lag-time before tubulin assembly, rate of assembly or the maximum amount of polymerization achieved. It is concluded that an impairment in hepatic microtubule assembly is not responsible for the development of the chlorinated alkane-induced fatty liver.
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PMID:The role of microtubules in chlorinated alkane-induced fatty liver. 357 42

An experimental model for monitoring rat liver function during protracted exposure to hepatotoxic agents is proposed. Owing to their invasiveness, the models usually employed are appropriate for studying the mechanism of action of toxic substances, but do not allow the liver situation to be followed over the course of time. The need to sacrifice animals to determine liver triglycerides-one of the key parameters in the progress of toxic damage- reduces the possibility of following such progress in the same animals. This study describes the testing of a model for monitoring three basic parameters of liver injury: cytolysis, steatosis and metabolic deficiency of the liver. CCl4 has been chosen as model-hepatotoxin. Steatosis is determined by evaluating the triglyceride content of small specimens of liver, obtained through open-field biopsies, which appear to be representative of the whole liver. Fatty liver is paralleled by the block in Triton-induced hypertriglyceridaemia. Determination of serum triglycerides derives from a very poorly invasive technique which can be repeated several times. The combination of these tests with the assessment of both the cytolysis (ALT and SDH release into the circulation) and the impairment of the efficiency of liver microsomal enzymes (TMO clearance), seems to offer a reliable experimental procedure in predicting the hepatotoxic effect of xenobiotics.
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PMID:A model for monitoring changes in liver function. 379 13

The mode of action of malotilate in normalizing serum cholesterol in hypocholesterolemic rats with fatty liver was examined by determination of biosynthesis, catabolism and excretion of cholesterol. Fatty liver was produced by subcutaneous injection of CCl4 at the dose of 1 ml/kg into male rats (SLC-SD) twice a week for 3 weeks. Daily administration of malotilate (100 mg/kg) in rats with hypocholesterolemia resulted in a rapid normalization of lowered serum cholesterol. Such a recovery of cholesterol level in serum coincided in time with normalization of the decreased cholesterol level of each lipoprotein fraction, VLDL-triglycerides secretion and the decreased apolipoprotein A1 value. Histopathological improvement in liver was also confirmed by a decrease in the size of fat droplets stored within the hepatocytes. The malotilate treatment gave a tendency to facilitate hepatic cholesterol synthesis in rats with fatty liver. Malotilate at a concentration of 0.5-2 micrograms/ml also stimulated cholesterol biosynthesis in cultured normal hepatocytes. The drug had the action to accelerate the catabolic excretion of 3H-labeled cholesterol into feces. These results suggest that the mode of action by which serum cholesterol is normalized in rats with fatty liver is probably due to a stimulative effect of malotilate on hepatic cholesterol synthesis and cholesterol secretion from the liver.
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PMID:Action of malotilate on reduced serum cholesterol level in rats with carbon tetrachloride-induced liver damage. 393 40

The therapeutic effect of diisopropyl 1,3-dithiol-2-ylidenemalonate (NKK-105) on the fatty liver induced by carbon tetrachloride (CCl4) was studied. The recovery from elevated liver triglyceride levels induced by CCl4 required over 20 days in 35 week-old rats, but 14 days in 6 week-old rats. This indicates that 35 week-old rats are useful for studying the therapeutic effect of NKK-105 on fatty liver. In rats with CCl4-induced fatty liver, NKK-105 lowered the hepatic triglyceride level, accelerated the rate of triglyceride release from the liver, enhanced the incorporation of 14C-leucine into microsomal protein, and increased the RNA content in microsomes. These data suggest that NKK-105 exerts a curative effect on CCl4-induced fatty liver by improving the impaired protein synthesis and by promoting lipoprotein secretion.
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PMID:Effect of diisopropyl 1,3-dithiol-2-ylidenemalonate (NKK-105) on fatty liver induced by carbon tetrachloride. 725 41

Preliminary data on the liver damage following combined treatment with paracetamol and carbon tetrachloride in the rat are reported. Administration of a single dose of paracetamol (2000 mg/kg, os) was followed after 1 hour by an intraperitoneal injection of CCl4 (1.0 ml/Kg). Experiments in parallel were performed in rat given paracetamol or CCl4 alone. Our results indicate paracetamol induces a drastic decrease of hepatic GSH that appears in relation with a marked production of TBA-reacting compounds in liver tissue, while CCl4 does not modify the hepatic content of GSH and provokes a slight increase of TBA-reacting substances. Preventive treatment with paracetamol of rats intoxicated after 1 hour with carbon tetrachloride results in a partial protection against fatty liver and necrosis following haloalkane poisoning. On the other hand, the combined treatment with both the hepatotoxins was followed by a minor decrease of GSH. These data are discussed in considering a possible interaction of the two chemicals at the site of their activation.
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PMID:[Liver damage after paracetamol and carbon tetrachloride administration]. 744 87

The study investigates the effect of a singular dose of CCl4 (2.5 ml/kg) on the concentration of triacylglycerols in the liver and oxidative phosphorylation in hepatic mitochondria after 24, 72 hours, 2 and 4 weeks since CCl4 application. It was discovered that 24 and 72 hours after CCl4 application the concentration of triacylglycerols increased significantly and steatosis of the liver supervened. After 2 and 4 weeks the triacylglycerol concentration values reached the level of those of control. The hepatic steatosis disappeared. The indices of oxidative phosphorylation index of respiration control, oxygen consumption during stimulated respiration (state 3), oxygen consumption during basal respiration (state 4), and phosphorylation velocity decreased significantly after 24 and 72 hours after CCl4 application in all observed substrates--glutamate, pyruvate and jantarane. After 2 to 4 weeks the observed indices reached the level of values characteristic for healthy controls. The results have indicated that after the CCl4 toxic impairment the energy metabolism in hepatic mitochondria has been significantly impaired. This impairment, in spite of its severeness, was irreversible and hepatocytes were able to compensate it (Tab. 4, Ref. 33).
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PMID:[Oxidative phosphorylation in liver mitochondria after injury with carbon tetrachloride and during regeneration]. 781 46

The aim of the study was to investigate the effect of beta-aescin on the selected indices of sugar and lipid metabolisms in blood and hepatic tissue. The study was performed under the conditions of toxic impairment of the liver caused by carbon tetrachloride or hydrazinsulphate which were used in order to evoke experimentally the steatosis of the liver. The study investigated whether beta-aescin can cause deterioration of hepatic steatosis. Carbon tetrachloride was administered to rats by stomach probe in dosis of 2.5 ml per kg of body weight, or hydrazinsulphate in dosis of 2 mmol per kg of body weight, i.m.. Twenty-four hours after administration of these two substances beta-aescin water solution was administered in dosis of 10 mg per kg of body weight by means of stomach probe. The analysis of blood and liver tissue samples discovered that beta-aescin did not affect the metabolic indices, steatosis of the liver did not become more profound. (Tab. 2, Fig. 11, Ref. 23.)
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PMID:[The effect of beta-escin on metabolism in experimental liver steatosis in rats]. 788 66

Nicotinamide (NIC) is known to increase the synthesis of pyridine nucleotides and also to inhibit the hydrolysis of them to ADP-ribose, which in turn is involved in Ca2+ release from mitochondria via the ADP ribosylation of crucial mitochondrial proteins. In this work, we test the potential ability of NIC to be a late protective agent against CCl4-induced liver necrosis. We observed that 1 g/kg po NIC, 30 min before or 6 or 10 hr after CCl4 (1 ml/kg), given ip as a 20% (v/v) solution in olive oil, was able to significantly prevent the necrogenic effect of the hepatotoxin at 24 hr as evidenced by determination of isocitric dehydrogenase activity in plasma or by histological observation. NIC administration 6 hr after CCl4 prevented fatty liver induced by hepatotoxin at 24 hr. NIC did not modify CCl4-induced lipid peroxidation process at 1 hr after CCl4 and decreased the covalent binding of 14CCl4 to lipids. NIC decreased the levels of 14CCl4 reaching the liver when given 30 min before hepatotoxin but not when given 6 hr after it. NIC lowered body temperature of rats at 1, 3, and 6 hr and augmented it at 24 hr after CCl4. NIC concentrations in liver as determined by GC/MS/SIM analysis were 21 micrograms/g liver 1 hr after administration and 53 micrograms/g at 3 hr. Late preventive effects of NIC against CCl4 induced liver necrosis when given at 6 or 10 hr after CCl4 are compatible with the hypothesis that NIC restores mitochondrial ability for Ca2+ uptake. This hypothesis remains to be proved and is being further challenged in our laboratory.
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PMID:Nicotinamide late protective effects against carbon tetrachloride-induced liver necrosis. 795 79

In this study the hepatic lipoprotein lipase (LPL) activity was evaluated in adult female mice acclimatized at 5 degrees C and submitted to carbon tetrachloride (CCl4) or ethionine, in order to determine the possible role of this enzyme in the fatty liver. The results were compared with those obtained in mice kept at room temperature (27 degrees C) that received the same hepatoesteatosis inducing agent. In contrast to animals kept at room temperature, in cold acclimatized mice neither the enhancement of the LPL-liver activity by the action of CCl4 or ethionine occurred nor the development of fatty infiltration in the liver was observed. We conclude that the low temperature induced a protective effect against CCl4- or ethionine-induced fatty liver that was correlated with the no-increase of the hepatic LPL activity.
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PMID:On the mechanism of protective action of cold acclimatization against carbon tetrachloride- and ethionine-induced fatty liver. 810 93

The effects of alcohol on hepatic iron uptake and intestinal iron transport were studied in rats fed a nutritionally replete liquid diet containing varying quantities of ethanol. Results were compared with those from animals exposed to carbon tetrachloride (CCl4) to produce hepatocellular necrosis or a choline-deficient diet to produce steatosis and cirrhosis. A high ethanol intake for 4 or 10 weeks produced hepatic steatosis. CCl4 produced hepatocellular necrosis. Choline deficiency was associated with steatosis +/- cirrhosis. Intestinal iron transport was unaffected by ethanol, CCl4, or choline deficiency. Hepatic iron uptake was significantly depressed in rats consuming 11.7 g/kg/day ethanol (p < 0.01) for 4 weeks. Choline-deficient animals studied at 14 weeks also had significantly decreased hepatic iron uptake (p < 0.01); results were similar in the cirrhotic and noncirrhotic animals. Conversely, CCl4 exposure produced a significant 5-fold increase in hepatic iron uptake (p < 0.001). Results suggest that ethanol consumption, fatty liver, and cirrhosis are not responsible for any increase in iron absorption or of hepatic iron uptake in the rat model. Acute hepatocellular injury is followed by increased hepatic iron uptake.
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PMID:Effects of alcohol, carbon tetrachloride, and choline deficiency on iron metabolism in the rat. 827 76


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