Fatty Acid Oxidation in Hepatic Peroxisomes and Mitochondria after Treatment of Rats with Di(2‐ethylhexyl)phthalate

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Abstract
Rats were fed a diet containing di(2-ethylhexyl)-phthalate, which increases the number of peroxisomes and mitochondria in the liver. This proliferation does not change the ratio of phospholipid to protein in mitochondria or microsomes, but causes certain changes in the fatty acid composition of the phospholipids. The highest rates of peroxisomal and mitochondrial .beta.-oxidation are obtained with 12:0 and 16:0 fatty acids as substrates, respectively. A 3-4 fold increase in the rate of .beta.-oxidation by both organelles is caused by DEHP treatment, but there are no qualitative changes in the relative rates of oxidation of individual fatty acids. Short- and medium-chain carnitine acyltransferases in peroxisomes, microsomes and mitochondria, as well as the mitochondrial long-chain carnitine acyltransferase are induced to various extents. These results indicate that the increased .beta.-oxidation of fatty acids caused by phthalate treatment involves the same peroxisomal and mitochondrial pathways which operate under normal conditions.

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