Hepatic content of coenzyme Q in rats with experimental liver damage and diabetes.

In 1957, Morton et at. (1) isolated a substance having the absorption maxima at 272 and 400 mƒÊ using paper chromatography from the lipid fraction of rat liver, and found that the hepatic content of this substance increased remarkably in the rats with vitamin A deficiency. Isler et at. (2) established the molecular structure of the compound including quinone nucleus with similar absorption characteristics after analyzing the crystal isolated from pork heart. Lester et at. (3) observed that this quinone substance could be reduced and oxidized in the presence of respiratory enzymes. Subsequent studies established the position of this substance in the electron transport system of mitochondria and role as the functional link between the flavoprotein and cytochrome c1. This new compound was named ubiquinone by Morton et at, and coenzyme Q (CoQ) by Lester et at. independently. It has been known that the liver of the animals with CCl4 poisoning has the disturbance in the oxdation of various substances and that the content of several vitamins or coenzymes related to such oxidative pathways is reduced. Previously our collaborators reported that the hepatic content of pantothenic acid, biotin and thioctic acid decreased in the rats with CCl4 poisoning compared with that in normal rats (4-6). The present study deals with the change in the content and the intracellular distribution of CoQ in the liver of rats with experimental liver damage and diabetes.