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Peroxisomal‐microsomal communication in unsaturated fatty acid metabolism
Author(s) -
Baykousheva Svetla P.,
Luthria Devanand L.,
Sprecher Howard
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)00565-q
Subject(s) - peroxisome , microsome , acyltransferase , acylation , chemistry , biochemistry , substrate (aquarium) , acyl coa , metabolism , fatty acid , microsoma , beta oxidation , enzyme , biology , catalysis , ecology , gene
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‐ 14 C]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‐ 14 C]7,10,13,16–22:4, but not from [3‐ 14 C]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.