The effect of the prostaglandin analogue - misoprostol on rat liver mitochondria after chronic alcohol feeding

Długosz, Jan; Korsten, Mark A.; Lieber, Charles S.

doi:10.1016/0024-3205(91)90080-u

Cited by 19 publications

(2 citation statements)

References 40 publications

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“…Thus, they concluded that PGE 2 increased hepatic DNA synthesis and regeneration in normal rat liver and overcame their inhibition when ethanol was given after partial hepatectomy. Dlugosz et al 30 ) fed rats with ethanol for 5 week and the rats developed functional alterations of hepatic mitochondira and steatosis of the liver. This study indicates that, although the mechanism of action of misoprostol is unknown, impairment of rat liver mitochondrial respiratory function in chronic injury can be partially prevented or corrected by treatment with the synthetic prostaglandin E 1 derivative misoprostol.…”

Section: Discussionmentioning

confidence: 99%

Effects of Prostaglandins on Ethanol Damage in Primary Cultured Rat Hepatocytes

Yang¹,

Choi²,

Kim³

et al. 1998

Korean J Intern Med

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ObjectivesSeveral reports demonstrated that ethanol administration impairs the DNA synthesis in rat hepatocytes. Also, It has been demonstrated that prostaglandin (PG) helps prevent membrane damage by hepatotoxic chemicals, in this study, the authors examined PG’s effects on the toxicity of ethanol in the primary culture of rat regenerations.MethodsWe examined two kinds of parameters, i.e., DNA synthesis and lipid peroxidation in the primary culture of rat hepatocytes. Hepatocytes were isolated by the collagenase perfusion method. The rate of DNA synthesis was determined by pulse-labelling cultured cells with [3H]-thymidine. Incorporation of [3H]-thymidine was determined by liquid scintillation spectrophotometer. DNA content was measured by the fluorescence spectrophotometer. The lipid peroxidation was assayed with spectrophotometer.ResultsThe results were as follows: 1) PG family (PGA1, PGD2, PGE1, PGE2, PGG2a, PGI2 & Thromboxane B2) stimulated the DNA synthesis of hepatocytes (especially PGD2 and PGE1), 2) ethanol decreased DNA synthesis by clear dose-dependent manner, 3) the combined treatment of PGD2 or PGE1, prevents the decreasing of DNA synthesis, which was induced by ethanol, 4) in ethanol treatment, lipid peroxidation was decreased significantly, but PGD2, PGE1 and PGA1 were not affected, and 5) PGD2, PGE1 and PGA1 decreased lipid peroxidation with ethanol, significantly.ConclusionsFrom these results, we concluded that PG could be useful for the treatment of degenerative liver disease and alcohol-induced liver disease in the assumption that further studies on the action mechanims of PG will continue.

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Section: Discussionmentioning

confidence: 99%

Effects of Prostaglandins on Ethanol Damage in Primary Cultured Rat Hepatocytes

Yang¹,

Choi²,

Kim³

et al. 1998

Korean J Intern Med

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“…Partially prevented impact of chronic alcoholic injury on liver mitochondrial respiratory function; reduced activity of alanine aminotransferase, ␥-glutamyl transpeptidase, and ammonia in blood and liver tissues. 164…”

Section: Ethanol Hepatotoxicity Ratsmentioning

confidence: 99%

Misoprostol Therapeutics Revisited

2001

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Misoprostol, a prostaglandin E1 analog, is a racemate of four stereoisomers. On administration it rapidly de-esterifies to its active form, misoprostolic acid. Misoprostolic acid is 85% albumin bound and has a half-life of approximately 30 minutes. It is excreted in urine as inactive metabolites. No significant drug interactions have been reported. Besides its gastrointestinal protective and uterotonic activities, misoprostol regulates various immunologic cascades. It inhibits platelet-activating factor and leukocyte adherence, and modulates adhesion molecule expression. It protects against gut irradiation injury, experimental gastric cancer, enteropathy, and constipation. It improves nutrient absorption in cystic fibrosis. Misoprostol has utility in acetaminophen and ethanol hepatotoxicity, hepatitis, and fibrosis. It is effective in asthmatics and aspirin-sensitive asthmatic and allergic patients. It lowers cholesterol and severity of peripheral vascular diseases, prolongs survival of cardiac and kidney transplantation, synergizes cyclosporine, and protects against cyclosporine-induced renal damage. It works against drug-induced renal damage, interstitial cystitis, lupus nephritis, and hepatorenal syndrome. It is useful in periodontal disease and dental repair. Misoprostol enhances glycosoaminoglycan synthesis in cartilage after injury. It prevents ultraviolet-induced cataracts and reduces intraocular pressure in glaucoma and ocular hypertension. It synergizes antiinflammatory and analgesic effects of diclofenac or colchicine and has been administered to treat trigeminal neuralgic pain. It reduces chemotherapy-induced hair loss and recovery time from burn injury, and is effective in treating sepsis, multiple sclerosis, and pancreatitis.

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Effects of ethanol on prostanoid production by liver fat-storing cells

Flisiak

Baraona

et al. 1993

Hepatology

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Fat-storing cells participate in the development of alcoholic liver disease. To study possible effects of ethanol on prostaglandin metabolism by fat-storing cells, we isolated them from normal rat liver. Cultured fat-storing cells produced substantial amounts (DNA, about 2 ng/micrograms every 24 hr) of prostaglandin E2 and prostaglandin I2 (measured as 6-keto prostaglandin F1 alpha) but no significant amounts of prostaglandin F2 alpha. This production was markedly enhanced by the addition of ethanol in concentrations likely to occur in the blood during alcohol consumption. We confirmed the presence of class 1 alcohol dehydrogenase activity and isoenzymes in the cytosol of cultured fat-storing cells in their second passage. The stimulatory effect of ethanol was inhibited by 4-methylpyrazole (an alcohol dehydrogenase inhibitor), exaggerated by disulfiram (an aldehyde dehydrogenase inhibitor) and reproduced by concentrations of acetaldehyde likely to occur in the liver. Thus, our results indicate that fat-storing cells produce vasodilatory prostaglandins and that this production is enhanced by the acetaldehyde that results from the oxidation of ethanol catalized by alcohol dehydrogenase present in these cells.

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The effect of the prostaglandin analogue - misoprostol on rat liver mitochondria after chronic alcohol feeding

Cited by 19 publications

References 40 publications

Effects of Prostaglandins on Ethanol Damage in Primary Cultured Rat Hepatocytes

Effects of Prostaglandins on Ethanol Damage in Primary Cultured Rat Hepatocytes

Misoprostol Therapeutics Revisited

Effects of ethanol on prostanoid production by liver fat-storing cells

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