Effects of acute ethanol intoxication on [3H]palmitic acid transport through hepatocyte Golgi apparatus.
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Biomedical subjects
Publications and source records attributed to G Nanni.
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The action of cis-2-hydroxy-2-phenyl-cyclohexanecarboxilic acid (cicloxilic acid) on the concentration of triglycerides in the subcellular compartments of the liver was investigated in acutely ethanol-intoxicated rats. Cicloxilic acid is able to significantly reduce the accumulation of neutral fats in the homogenate and in the cytosol and to shorten the steatosis regression time. The triglyceride content in total microsomes results slightly higher in the animals treated with cicloxilic acid than in those treated with ethanol only. The data are discussed in relation to the pathogenesis of ethanol fatty liver and to the possible mechanism of action of cicloxilic acid.
Liver mitochondria from acute ethanol intoxicated rats show a highly significant uncoupling of oxidative phosphorylation. cis-2-Hydroxy-2-phenyl-cyclohexanecarboxylic acid (cicloxilic acid) early normalizes the P/O ratio and, therefore, the mitochondrial energy producing mechanisms. The significance of these phenomena and the possible role of cicloxilic acid on mitochondrial energy-production are discussed.
cis-2-Hydroxy-2-phenyl-cyclohexanecarboxilic acid (cicloxilic acid) modifies the rat's hepatocyte intracellular movements of 3H-palmitic acid in the course of fatty liver by acute ethanol intoxication. It counteracts the impairment of radioactive lipid uptake due to ethanol treatment and promotes the early and complete release of the radioisotope inhibited by ethanol. The relevance of these results to the role of changes in the intracellular transport systems in the pathogenesis of ethanol steatosis is discussed. This and previous studies show that cicloxilic acid acts by stimulating the intracellular lipoprotein transport probably preventing by this mechanism the ethanol induced liver injury.
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