Ethanol-Induced Fatty Liver in Rats: Effects of Pyrazole and Glucose

Domanski, Robert E.; Rifenberick, David H.; Stearns, Frank M.; Scorpio, Ralph M.; Narrod, Stuart A.

doi:10.3181/00379727-138-35823

Cited by 15 publications

(2 citation statements)

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“…As regards treatment with pyrazole, a competitive ADH inhibitor (Goldberg and Rydberg, 1969), we were not able to detect any protection against ethanol. This is in agreement with previous observations of Bustos et aZ (1970), but in contrast with the data of Domanski (1971) who reported that pyrazole slightly inhibited acute fatty liver induced by ethanol in female rats and, as reported by Morgan and Di Luzio (1970), completely prevented hepatic triglyceride accumulation in male rats in the same experimental conditions.…”

Section: Discussionsupporting

confidence: 93%

Ethanol‐induced hepatotoxicity; experimental observations on the role of lipid peroxidation

Torrielli

Gabriel

Dianzani

1978

The Journal of Pathology

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Hepatic lipid peroxidation in vivo or in vitro as measured by UV absorption spectra of microsomal lipids or by production of TBA-reacting substances by whole liver homogenates, was studied after acute or during prolonged administration of ethanol. No evidence of peroxidative derangement of liver microsomal lipids in vivo was detected in either experimental situation, while the production of TBA-reacting substances by pooled liver homogenates incubated in vitro appeared slightly increased. Treatment with reduced glutathione (GSH and 2-mercaptopropionylglycine (2-MPG) was able to reduce fatty liver in acute and prolonged ethanol dosing, as well as the production of TBA-reacting compounds. Similar effects were obtained with 3-amino-1,2,4-triazole which was assayed only in acute experiments. By contrast, hepatic triglyceride accumulation induced by a single intoxicating dose of ethanol was not affected by preventive treatment with pyrazole which seemed to act as a pro-oxidant agent as far as the production of TBA-reacting substances is concerned. The role of lipid peroxidation as a pathogenic mechanism for acute and chronic ethanol-induced hepatotoxicity is discussed in relation to the action of anti-oxidant compounds which are active in preventing liver injury. It is concluded that lipid peroxidation is unlikely to be an important mechanism in alcohol hepatotoxicity.

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Section: Discussionsupporting

confidence: 93%

Ethanol‐induced hepatotoxicity; experimental observations on the role of lipid peroxidation

Torrielli

Gabriel

Dianzani

1978

The Journal of Pathology

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“…They are, however, in conflict with other experiments in which the accumulation of triglycerides in the liver could be prevented by pyrazole [26] and methylpyrazole [5]. The discrepancy between these findings is hardly to explain, but it seems that under different experimental conditions different mechanisms are responsible for the development of the fatty liver [10,21].…”

Section: Discussioncontrasting

confidence: 55%

Effects of pyrazole on ethanol-induced changes in hepatic triglyceride and glycerol-1-phosphate contents and on esterified and non-esterified fatty acids in the blood

Estler

1974

Res. Exp. Med.

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Summary.Within 2 hrs after a single dose of 4 mg/g ethanol i.v. the glycerol-lphosphate content, the glycerol-l-phosphate/dihydroxyacetone phosphate ratio and the triglyceride content of the liver of mice rises significantly. At the same time the non-esterified fatty acids in the blood are slightly elevated and the esterified fatty acids in the blood slightly decreased. 340 ~g/g pyrazole i.p., which completely prevent the degradation of ethanol, prevent also the increase of the glycerol-l-phosphate content and of the glycerol-l-phosphate/dihydroxyacctone phosphate ratio but are without influence on the accumulation of triglyceridcs in the liver and on the non-esterified fatty acids in the blood. It is concluded from these results that the accumulation of fat in the liver produced by ethanol is not causally connected to ethanol oxidation or to concomitant metabolic changes (e.g. rise of the NADH/NAD ratio) but must be ascribed to toxic effects of ethanol itself.

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Ethanol and Lipid Disorders, Including Fatty Liver, Hyperlipemia, and Atherosclerosis

Lieber¹

1992

Medical and Nutritional Complications of Alcoholism

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Ethanol-Induced Fatty Liver in Rats: Effects of Pyrazole and Glucose

Cited by 15 publications

References 1 publication

Ethanol‐induced hepatotoxicity; experimental observations on the role of lipid peroxidation

Ethanol‐induced hepatotoxicity; experimental observations on the role of lipid peroxidation

Effects of pyrazole on ethanol-induced changes in hepatic triglyceride and glycerol-1-phosphate contents and on esterified and non-esterified fatty acids in the blood

Ethanol and Lipid Disorders, Including Fatty Liver, Hyperlipemia, and Atherosclerosis

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