Total and peroxisomal fatty acid oxidation by liver homogenates from autopsied Reye's and control subjects.
To determine whether the accumulation of liver triglyceride in Reye's syndrome could be due to a block in beta-oxidation of the fatty acids, the ability of Reye's and control liver homogenates from samples obtained at autopsy to oxidize fatty acids was examined. Total fatty acid oxidation as measured by oxidation of [1-14C]oleoyl CoA, which mostly represents mitochondrial activity, was comparable between the groups. Peroxisomal fatty acid oxidation was, likewise, similar despite the reported increase in the numbers and sizes of these organelles. This disparity could not be explained by an artifactual dilution of product by accumulated endogenous substrate. Inference is made that active peroxisomal beta-oxidation may contribute to the increased short chain fatty CoA content of liver which was reported earlier.
D000214:Acyl Coenzyme A / Q000378:metabolism*; D001344:Autopsy; D002250:Carbon Radioisotopes; D006801:Humans; D007700:Kinetics; D008099:Liver / Q000378:metabolism*; D008830:Microbodies / Q000378:metabolism*; D010084:Oxidation-Reduction; D011865:Radioisotope Dilution Technique; D012016:Reference Values; D012202:Reye Syndrome / Q000378:metabolism*
D000214:Acyl Coenzyme A; D002250:Carbon Radioisotopes; C017585:oleoyl-coenzyme A