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Item Arachidonic acid formed by peroxisomal β-oxidation of 7,10,13,16- docosatetraenoic acid is esterified into 1-acyl-sn-glycero-3-phosphocholine by microsomes(American Society for Biochemistry and Molecular Biology, Inc., 1994) Baykousheva, S. P.; Luthria, D. L.; Sprecher, H.Peroxisomal beta-oxidation of linoleic acid and arachidonic acid was depressed when 1-palmitoyl-sn-glycero-3-phosphocholine and microsomes were included in incubations. This reduction was due to the esterification of the substrate into the acceptor by microsomal 1-acyl-sn-glycero-3- phosphocholine acyltransferase. The first cycle of the beta-oxidation of 7,10,13,16-docosatetraenoic acid was independent of 1-acyl-sn-glycero-3-phosphocholine and microsomes. However, when arachidonate was produced it was esterified rather than serving as a substrate for continued beta-oxidation. When arachidonate and linoleate were incubated with peroxisomes alone, 2-trans-4,7,10-hexadecatetraenoic acid and 2-trans-4-decadienoic acid were the respective end products of beta-oxidation. 2-Oxo-8,11-heptadecadienone, a catabolite produced from linoleate, was most likely a nonenzymatic decarboxylation product of 3-oxo-9,12-octadecadienoic acid. In addition to the termination of beta-oxidation by microsomal-peroxisomal communication, our results with linoleate and arachidonate suggest that the reaction catalyzed by 2-trans-4-cis-dienoyl-CoA reductase is the control step in double bond removal. In addition, the beta-ketothiolase step may play a regulatory role in the peroxisomal beta-oxidation of linoleate but not arachidonate or 7,10,13,16-docosatetraenoic acid.Item Regulation of the biosynthesis of 4,7,10,13,16-docosapentaenoic acid(1997) Mohammed, B. S.; Luthria, D. L.; Baykousheva, S. P.; Sprecher, H.It is now established that fatty acid 7,10,13,16-22:4 is metabolized into 4,7,10,13,16-22:5 as follows: 7,10,13,16-22:4-->9,12,15, 18-24:4-->6,9,12,15,18-24:5-->4,7,10,13,16-22:5. Neither C24 fatty acid was esterified to 1-acyl-sn-glycero-3-phosphocholine (1-acyl-GPC) by microsomes, whereas the rates of esterification of 4, 7,10,13,16-22:5, 7,10,13,16-22:4 and 5,8,11,14-20:4 were respectively 135, 18 and 160 nmol/min per mg of microsomal protein. About four times as much acid-soluble radioactivity was produced when peroxisomes were incubated with [3-14C]9,12,15,18-24:4 compared with 6,9,12,15,18-24:5. Only [1-14C]7,10,13,16-22:4 accumulated when [3-14C]9,12,15,18-24:4 was the substrate, but both 4,7,10,13,16-22:5 and 2-trans-4,7,10,13,16-22:6 were produced from [3-14C]6,9,12,15, 18-24:5. When the two C24 fatty acids were incubated with peroxisomes, microsomes and 1-acyl-GPC there was a decrease in the production of acid-soluble radioactivity from [3-14C]6,9,12,15, 18-24:5, but not from [3-14C]9,12,15,18-24:4. The preferential fate of [1-14C]4,7,10,13,16-22:5, when it was produced, was to move out of peroxisomes for esterification into the acceptor, whereas only small amounts of 7,10,13,16-22:4 were esterified. By using 2H-labelled 9,12,15,18-24:4 it was shown that, when 7,10,13,16-22:4 was produced, its primary metabolic fate was degradation to yield esterified arachidonate. Collectively, the results show that an inverse relationship exists between rates of peroxisomal beta-oxidation and of esterification into 1-acyl-GPC by microsomes. Most importantly, when a fatty acid is produced with its first double bond at position 4, it preferentially moves out of peroxisomes for esterification to 1-acyl-GPC by microsomes, rather than being degraded further via a cycle of beta-oxidation that requires NADPH-dependent 2,4-dienoyl-CoA reductase.