Library Faculty/Staff Scholarship and Research

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Author: search.filters.author.Sprecher, Howard

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    Pathways for the biosynthesis of polyunsaturated fatty acids
    (1996) Sprecher, Howard; Luthria, Devanand; Baykousheva, Svetla P.; Mohammed, Selma B.
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    Peroxisomal-microsomal communication in unsaturated fatty acid metabolism
    (Elsevier, 1995) Baykousheva, Svetla P.; Luthria, Devanand L.; Sprecher, Howard
    The addition of 1-acyl-sn-glycero-3-phosphocholine (1-acyl-GPC) to peroxisomes decreased the production of acid-soluble radioactivity formed by β-oxidation of [1-14C]arachidonate due to substrate removal by esterification into the acceptor. This peroxisomal-associated acyl-CoA:1-acyl-GPC acyltransferase activity was due to microsomal contamination. The production of acid-soluble radioactivity from [1-14C]7,10,13,16–22:4, but not from [3-14C]7,10,13,16–22:4 was independent of 1-acyl-GPC, with and without microsomes. By comparing rates of peroxisomal β-oxidation with those for microsomal acylation, it was shown that the preferred metabolic fate of arachidonate, when added directly to incubations, or generated via β-oxidation, was esterification by microsomal 1-acyl-GPC acyltransferase, rather than continued peroxisomal β-oxidation.
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    The role played by β-oxidation in unsaturated fatty acid biosynthesis
    (1994) Sprecher, Howard; Baykousheva, Svetla
    The authors hypothesized that a role for peroxisomes might be to chain shorten fatty acids but that the products would be transported to the endoplasmic reticulum where they would be esterified into lipids. Results showed that when microsomes and 1-acyl-sn-glycero-3-phosphocholine are added to peroxisomes that competing reactions take place, i.e. β-oxidn. and esterification.
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    Regulation of the biosynthesis of 4,7,10,13,16-docosapentaenoic acid
    (Portland Press, 1997-09-01) Mohammed, B. Selma; Luthria, Devanand L.; Bakousheva, Svetla P.; Sprecher, Howard
    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 C#% fatty acid was esteri®ed to 1-acyl-sn-glycero-3-phosphocholine (1-acyl- GPC) by microsomes, whereas the rates of esteri®cation 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-"%C]- 9,12,15,18-24:4 compared with 6,9,12,15,18-24:5. Only [1-"%C]7,10,13,16-22:4 accumulated when [3-"%C]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-"%C]6,9,12,15,18-24:5. When the two C#% fatty acids were incubated with peroxisomes, microsomes and 1-acyl-GPC there was a decrease in the production of acid-soluble radioactivity from [3-"%C]6,9,12,15,18-24:5, but not from [3-"%C]9,12,15,18-24:4. The preferential fate of [1-"%C]4,7,10,13,16-22:5, when it was produced, was to move out of peroxisomes for esteri®cation into the acceptor, whereas only small amounts of 7,10,13,16-22:4 were esteri®ed. By using #H-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 esteri®ed arachidonate. Collectively, the results show that an inverse relationship exists between rates of peroxisomal b-oxidation and of esteri®cation into 1-acyl-GPC by microsomes. Most importantly, when a fatty acid is produced with its ®rst double bond at position 4, it preferentially moves out of peroxisomes for esteri®cation to 1-acyl-GPC by microsomes, rather than being degraded further via a cycle of b-oxidation that requires NADPH-dependent 2,4-dienoyl-CoA reductase.