Role of gastric emptying on ethanol poisoning in rats

Intraperitoneal glucose was demonstrated to significantly inhibit the absorption of ethanol ( 2 g/kg) administered orally to rats. The effect was due to slowed emptying of the stomach, verified by analysis of the stomach contents and of blood enthanol levels. The observation agrees with previous findings, according to which the rate of stomach emptying is inversely related to the blood glucose level. However, when glucose was given intravenously 15 minutes after oral administration of a lethal dose of ethanol (12.5 g/kg) no significant inhibition of ethanol absorption could be observed. Intravenous propantheline, pyrithioxine and methylene blue were also unable to prolong the survival time or to influence the lethal blood ethanol concentration (about 170 mmol/l) of the enthanol-poisoned rats.     

Phosphoinositides kinases in brain aging and amyloid beta neurotoxicity

Brain platelet-activating factor (PAF) is a lipid mediator involved in neurotransmission and in LTP. It has been reported that the induction of LTP by high frequency stimulation increases the activity of the enzymes responsible for its synthesis by a still unknown mechanism ( 1 ). One of the two biosynthetic pathways is Ca²⁺-dependent and transforms a membrane ether phospholipid into PAF by a sequence of two reactions being the first one, catalyzed by a phospholipase A₂ (PLA₂), rate limiting. Overproduction of PAF, taking place in pathological conditions, contributes to brain damage. Various PLA₂s are present in brain tissue and, particularly, sPLA₂-IIA is very likely involved in the production of PAF as its expression increases in pathological conditions. Recently, we have found the release of sPLA₂-IIA from rat brain cortex mitochondria and its association with nuclear membranes, which might be an intracellular target for the enzyme.     

Changes in the blood of Wistar rats in acute poisoning with ethanol and acetaldehyde

1. The purpose of the study was to investigate the effect of ethanol and acetaldehyde on the erythrocyte and leucocyte system of Wistar rats. 2. Administration of the ethanol or acetaldehyde caused a considerable drop in the number of erythrocytes, haemoglobin level and haematocrit value in rats. 3. The mean erythrocyte volume was smaller after only 0.5 hr of exposure to ethyl alcohol. 4. The solutions used caused changes in the leucocyte system expressed in distinct neutrophilic leucocytosis. 5. Changes in the leucogram were reflected in the increase in the leucocyte index. 6. The degree of intensity of changes in both the erythrocyte and leucocyte system point to the greater toxicity of ethyl alcohol intoxication than is the case of acetaldehyde in a toxically corresponding dose (i.e. 0.5 and 5 g/kg body wt respectively).     

DNA synthesis in the brain and liver of rats in various stages of postnatal development]

The intensity of incorporation of 3H- and 14C-thymidine in the brain and liver DNA in rats of different ages was investigated. It was proved that both the replicative and oxyurea-resistant DNA synthesis might proceed in the rat brain cells. The intensity of these processes changes sharply during postnatal development.     

Effects of ethanol and limontar in the antenatal period of development on lipid peroxidation process and antioxidant defense system in the brain and liver tissue of fetal and newborn rats]

The process of lipid peroxidation and the system of antioxidant defense in brain and liver of fetuses on the 20th day of gestation and 1 day old rats after antenatal exposure to ethanol and limontar were studied. It was shown that antenatal exposure to ethanol led to activation of the process of lipid peroxidation in brain and to inhibition of of the enzyme system of antioxidant defense in liver of fetal and newborn rats. Limontar promoted the normalization of both the process of lipid peroxidation and the system of antioxidant defense.     

A proteomic analysis of liver after ethanol binge in chronically ethanol treated rats

ABSTRACT: BACKGROUND: Binge ethanol in rats after chronic ethanol exposure augments necrosis and steatosis in the liver. In this study, two-dimensional gel electrophoresis proteomic profiles of liver of control, chronic ethanol, control-binge, and chronic ethanol- binge were compared. RESULTS: The proteomic analysis identified changes in protein abundance among the groups. The levels of carbonic anhydrase isoform 3 (CA3) were decreased after chronic ethanol and decreased further after chronic ethanol-binge. Ethanol binge alone in control rats had no effect on this protein suggesting its possible role in increased susceptibility to injury by binge after chonic ethanol treatment. A protein spot, in which both cytosolic isocitrate dehydrogenase (IDH1) and glutamine synthetase (GS) were identified, showed a small decrease after chronic ethanol binge but western blot demonstrated significant decrease only for glutamine synthetase in chronic ethanol treated rats. Level of gluathione S-transferase mu isoform (GSTM1) increased after chronic ethanol but the levels were lower after chronic ethanol-binge compared to chronic ethanol treatment. The protein levels of basic form protein disulfide isomerase associated protein 3 (PDIA3) were significantly decreased and acidic forms were increased after chronic ethanol- binge but not in chronic ethanol treated rats or ethanol binge in control rats. CONCLUSIONS: Given the role of CA3, IDH1 and GST in oxidative stress; PDIA3 in protein quality, apoptosis and DNA repair; and decreased glutamine synthetase as a sensitive marker of pericentral liver injury; this proteome study of chronic ethanol-binge rat model identifies these proteins for the first time as molecular targets with potential role in progression of liver injury by binge ethanol drinking.     

Influence of ethanol on the liver metabolism of fed and starved rats

1. The influence of ethanol on the metabolism of livers from fed and starved rats has been studied in liver-perfusion experiments. Results have been obtained on oxygen consumption and carbon dioxide production, on glucose release and uptake by the liver and on changes in the concentrations of lactate and pyruvate and of β-hydroxybutyrate and acetoacetate in the perfusion medium. 2. Oxygen consumption and carbon dioxide production were lower in livers from starved rats than in livers from fed rats. Ethanol had no effect on the oxygen consumption of either type of liver. After the addition of ethanol to the perfusion medium carbon dioxide production ceased almost completely, the change being faster in livers from starved rats. 3. With livers from fed rats glucose was released from the liver into the perfusion medium. This release was slightly greater when ethanol was present. With livers from starved rats no release of glucose was observed, and when ethanol was added a marked uptake of glucose from the medium was found. A simultaneous release of glycolytic end products, lactate and pyruvate, into the medium occurred. 4. Acetate was the main metabolite accumulating in the perfusion medium when ethanol was oxidized. With livers from starved rats a slightly increased formation of ketone bodies was found when ethanol was present. 5. The lactate/pyruvate concentration ratio in the perfusion medium increased from 10 to 87 with livers from fed rats and from 20 to 171 with livers from starved rats when the livers were perfused with ethanol in the medium. The β-hydroxybutyrate/acetoacetate concentration ratio increased from 0·8 to 7·6 with livers from fed rats and from 1·0 to 9·5 with livers from starved rats when ethanol was added to the medium. 6. The effects of ethanol are discussed and related to changes in the redox state of the liver that produce new conditions for some metabolic pathways.     

Effect of phenazepam on the ethanol demand of rats]

The new Soviet tranquilizer phenazepam given to rats intraperitoneally at a dose of 1 mg/kg daily was shown to be capable of suppressing ethanol addiction produced by 2-month intake of 5% ethanolic solution as the only source of liquid. The mechanism of this effect is likely to be related to the changes in the activity of the neurosecretory centers of the hypothalamus. The phenazepam in the treatment of chronic alcoholism.     

Histochemical and cytologic changes in the liver in experimental poisoning and subsequent pregnancy]

In 275 white rats chronic intoxication was produced by injection of amidopyrine acetaldehyde and chloraldehyde derivatives for 4 months. Histochemical and electron microscopic investigations of the liver under the experimental conditions and subsequent pregnancy revealed certain changes in nucleic metabolism, glycogenolisis, in the content of sulfhydryl, disulfide, carboxylic groups of protein molecules. Decrease in activity of enzymes of Krebs cycle and pentosophosphate cycle proved the deep changes in hepatocytes at the level of oxidation-reduction processes and protein synthesis. Ultramicroscopic changes in the nucleus, in cytoplasmic network, mitochondria and local degenerative alterations determined the level of morphologic reconstructions in connection with the intoxication. As the liver performs a number of vital functions and is closely connected with regulatory systems of the organism, morphofunctional shifts in the organ affect unfavourably the system mother--fetus.     

Growth and liver morphology after long-term ethanol consumption of rats

Ethanol was administered to female and male Wistar rats by mixing it with their drinking water. Ethanol concentrations were gradually increased up to either 8% or 15%. Female rats receiving 8% ethanol in their drinking water consumed 5-13 g, males 4-10 g daily. The ethanol/total food caloric intake percentages were 13 to 20% and 9 to 15% for female and male rats, respectively. There was no difference in body weight and relative liver weight between treated rats and their controls. Female and male rats receiving 15% of ethanol in their drinking water consumed 8-14 g ethanol per kg body weight per day. The percentages of ethanol/total food caloric intake were stabilized at about 25% for both sexes. Growth of the rats differed only slightly from controls; a tendency for a higher increase of body weight of the control rats was found. No difference in relative liver weight between ethanol-treated and control rats was observed. Microscopic examinations revealed that the ethanol treatment resulted in fat accumulation in the liver cells. A proliferation of the Smooth Endoplasmic Reticulum (SER) was more marked in the 15% dosed rats than in the 8% dosed rats and more distinct in female rats than in male rats in both dosage groups.     

The effect of ethanol on the bile-secreting function of the liver in rats

The effect of long-term application of ethanol on the biochemical composition of rat bile has been studied. These results have been compared with the changes of activity of hepatic microsomal enzymes and ultrastructure of hepatocytes. The changes of biliary lipid synthesis and secretion have been shown to reflect the change of microsomal metabolic functions and to be accompanied by liver destruction processes.     

Alpha-fetoprotein in the liver of embryonic and newborn rats]

The localization of alpha-fetoprotein in the liver of embryos and newborn Wistar rats was determined by the method of fluorescent antibodies. This protein was found in the cytoplasm of some hepatocytes, endothelium of blood vessels and erythroid blood cells of embryos and new born rats. It was never found in the blood-forming and Kupffer cells of the liver, as well as in the epithelium of bile ducts. The hepatocytes containing this protein were located in the liver lobes near the central veins. Their number and the intensity of fluorescence decreased with the age of animals.     

Effect of acute alcoholic and acetaldehyde poisoning on lipid metabolism in the rat liver]

Lipid metabolism in the liver of rats in acute alcohol (25% solution, intraperitoneally, 4 g/kg, 30 minutes) and acetaldehyde (5% solution, intraperitoneally, 0.266 g/kg, 30 minutes) intoxication has been studied. It has been revealed that with acute injection of ethanol into the livers of experimental animals the level of cholesterol is decreased, the content of triacylglycerols and phosphatidylethanolamine is increased. Analogous changes in the concentration of lipid fractions have been also revealed after injection of acetaldehyde.     

Effects of lead poisoning on properties of brain mitochondria in young rats

When the litters were 14 days old, wistar rat pups received lead ions. The suckling mother was fed by a powdered laboratory chow containing lead carbonate (1%, 2%, 4%). The intoxication was going on for 3 days to 9 weeks. While lead-fed pups showed a decrease in body-weight gain and in neurologic development, lead ions were without effects on oxygen consumption, ADP-phosphorylation and activity of several enzymes of cerebral mitochondria. On the other hand, the important lead accumulation into cerebral mitochondria was in a straight ratio with lead doses in the feedings. To explain the in vivo data, the effects of lead acetate were investigated in vitro on brain mitochondria of young male wistar rats. Our findings indicate that lead ions alter mitochondrial respiration and ADP-phosphorylation and that inorganic phosphate has a protective effect.