Increases in tissue levels of ubiquinone in association with peroxisome proliferation

Rats were treated with various peroxisome proliferators and concomitant changes in ubiquinone levels were monitored. In addition to clofibrate and di(2-ethylhexyl)phthalate, acetylsalicylic acid, 2-ethylhexanoic acid, thyroxine and dehydroepiandrosterone were used as proliferators. Administration of these compounds increased the contents of ubiquinone in liver and, to some extent, in kidney and muscle. No change in corresponding valued for heart or brain were observed. The treatments did not influence cholesterol levels, but increased the amounts of dolichol in the liver to various extents. Treatment of rats with the catalase inhibitor aminotriazole increased the ubiquinone levels in kidney, heart and muscle but not in liver. Comparison of peroxisomal fatty acid beta-oxidation with ubiquinone amounts in liver homogenates after treatment with a number of peroxisome proliferators demonstrated a direct correlation between these two parameters. Subcellular fractionation of liver after peroxisome proliferation revealed that the ubiquinone level was increased in mitochondria and lysosomes which are the main compartments for this lipid, but an increase was also observed in both peroxisomes and microsomes. The increase in hepatic ubiquinone after treatment with various types of proliferators was related to the decrease in blood cholesterol level. These results show that the volume of the peroxisomal compartment and the ubiquinone content in animal tissues are interrelated.