Subcellular changes and apoptosis induced by ethanol in rat liver

Benedetti, Antonio; Brunelli, E.; Risicato, Roberto; Cilluffo, Teresa; Jézéquel, A.M.; Orlandi, F.

doi:10.1016/s0168-8278(88)80024-2

Cited by 93 publications

(46 citation statements)

References 16 publications

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“…Keywords: Ethanol consumption; Growth; Rats; Liver cytology; Liver pathology Received 6 June 1989;accepted II December 1989 Several methods of administration of ethanol to rats have been reported in the literature, varying from injection of daily doses (Farbiszewski et al, 1988)to synthetic liquid diets (Lieber & DeCarli, 1967, 1982French, 1968).Ethanol is often added to the drinking water (Thorpe & Shorey, 1965;Dobbins et al, 1972;Liu et al ,1975;Prasad et al, 1985;Vii.ii.nanen& Lindros, 1985;Nadkarni & D'Souza, 1988;Benedetti et al, 1988). In this paper a method of administering ethanol to rats via the drinking water is described.…”

Section: Discussionmentioning

confidence: 99%

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

Wiel

Duijf²,

Pertijs³

et al. 1990

Lab Anim

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SummaryEthanol 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 15070.Female rats receiving8070 ethanol in their drinking water consumed 5-13 g, males 4-10 g daily. The ethanol/total food caloric intake percentages were 13 to 20070and 9 to 15070for 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 15070 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 25070for 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 15070 dosed rats than in the 8% dosed rats and more distinct in female rats than in male rats in both dosage groups.

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Section: Discussionmentioning

confidence: 99%

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

Wiel

Duijf²,

Pertijs³

et al. 1990

Lab Anim

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“…Emerging data indicate that apoptosis occurs in several ethanol-treated hepatocytes, whereas ethanol per se did hepatobiliary diseases. 6 Benedetti et al 7 reported their morphonot increase the number of PI-positive hepatocytes. Fur-logical study which suggests that apoptosis occurs in rat liver thermore, combination of ethanol and DMA but not etha-after long-term ethanol feeding.…”

Section: Apoptosis Of Hepatocytes Hepatocytes Were Isolatedmentioning

confidence: 97%

“…[6][7][8] These previous Figure 10 shows representative fluoroimages of fluores-studies were conducted by using animal models of chronic cence in situ nick end label using the sections of rat liver. ethanol feeding.…”

Section: This Relation Indicates That In Hepatocytes In Which Ethanolmentioning

confidence: 99%

Oxidative stress-mediated apoptosis of hepatocytes exposed to acute ethanol intoxication

Kurose

1997

Hepatology

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“…It has been demonstrated that ethanol administration is linked to increased hepatocyte apoptosis in both clinical and experimental alcohol-induced liver injury in a variety of species of animals including rats, mice and minipigs [1][2][3][4][5][6][7][8][9][10][11][12][13]. Although much progress has been made in understanding the role of critical factors that may be involved, such as cytokines and oxidative stress, there is still no unified hypothesis to explain the pathogenesis of alcoholinduced apoptosis of hepatocytes.…”

Section: Introductionmentioning

confidence: 99%

Role of elevated S-adenosylhomocysteine in rat hepatocyte apoptosis: Protection by betaine

Kharbanda

Rogers²,

Mailliard

et al. 2005

Biochemical Pharmacology

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Previous studies from our laboratory have shown that ethanol consumption results in an increase in hepatocellular S-adenosylhomocysteine levels. Because S-adenosylhomocysteine is a potent inhibitor of methylation reactions, we propose that increased intracellular S-adenosylhomocysteine levels could be a major contributor to ethanol-induced pathologies. To test this hypothesis, hepatocytes isolated from rat livers were grown on collagen-coated plates in Williams' medium E containing 5% FCS and exposed to varying concentrations of adenosine in order to increase intracellular S-adenosylhomocysteine levels. We observed increases in caspase-3 activity following exposure to adenosine. This increase in caspase activity correlated with increases in intracellular S-adenosylhomocysteine levels and DNA hypoploidy. The adenosine-induced changes could be significantly attenuated by betaine administration. The mechanism of betaine action appeared to be via the methylation reaction catalyzed by betaine-homocysteine-methyltransferase. To conclude, our results indicate that the elevation of S-adenosylhomocysteine levels in the liver by ethanol is a major factor in altering methylation reactions and in increasing apoptosis in the liver. We conclude that ethanol-induced alteration in methionine metabolic pathways may play a crucial role in the pathologies associated with alcoholic liver injury and that betaine administration may have beneficial therapeutic effects. Published by Elsevier Inc.

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Subcellular changes and apoptosis induced by ethanol in rat liver

Cited by 93 publications

References 16 publications

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

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

Oxidative stress-mediated apoptosis of hepatocytes exposed to acute ethanol intoxication

Role of elevated S-adenosylhomocysteine in rat hepatocyte apoptosis: Protection by betaine

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