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Total and peroxisomal oxidation of various saturated and unsaturated fatty acids in rat liver, heart and m. quadriceps
Author(s) -
Reubsaet F. A. G.,
Veerkamp J. H.,
Trijbels J. M. F.,
Monnens L. A. H.
Publication year - 1989
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/bf02544539
Subject(s) - peroxisome , palmitic acid , arachidonic acid , linoleic acid , biochemistry , fatty acid , beta oxidation , oleic acid , chemistry , polyunsaturated fatty acid , enzyme , gene
Rates of total and peroxisomal fatty acid oxidation were estimated from the production of 14 C‐labeled CO 2 and acid‐soluble products from differently labeled [ 14 C]fatty acids, in the absence and presence of antimycinrotenone, in homogenates of liver, heart and m. quadriceps. Total and peroxisomal oxidation rates of palmitic, oleic and linoleic acid were 3–4 times higher than those of arachidonic and adrenic acid which had higher oxidation rates than those of lignoceric and erucic acid. The peroxisomal contribution to the oxidation of the last fatty acids was similar to or higher than that of palmitic acid. For all fatty acids tested in these tissues, the mitochondrial contribution to β‐oxidation was higher than the peroxisomal contribution. Production of 14 CO 2 and 14 C‐labeled, acid‐soluble metabolites from [13‐ 14 ]arachidonic acid indicated that polyunsaturated fatty acids can be chain‐shortened beyond their double bonds in m. quadriceps and heart as well as in liver. Although 2,4‐dienoyl‐CoA reductase requires NADPH, addition of this coenzyme did not influence arachidonic acid oxidation. Arachidonic acid oxidation was inhibited by palmitic acid in mitochondria and peroxisomes, but arachidonic acid had only a slight effect on palmitic acid oxidation.