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Dietary α‐linolenate suppresses endotoxin‐induced platelet‐activating factor production in rat kidney
Author(s) -
Ohhashi Kentaro,
Takahashi Tetsuya,
Tanabe Akiko,
Watanabe Shiro,
Okuyama Harumi
Publication year - 1999
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/s11745-999-334-3
Subject(s) - linolenate , platelet activating factor , chemistry , clinical chemistry , kidney , medicine , biochemistry , fatty acid , arachidonic acid , endocrinology , lipidology , biology , enzyme
In comparison with dietary high‐linoleate safflower oil, high α‐linolenate perilla oil decreased alkylacyl‐and alkenylacyl‐glycerophosphocholine (GPC) content in rat kidney by roughly 30 and 25%, respectively. The fatty acid composition was also modified by high α‐linolenate oil; arachidonic acid (AA) level in alkylacyl‐GPC, a platelet‐activating factor (PAF) precursor, decreased by 30% along with concomitant increases in the n‐3 fatty acid levels. PAF contents under resting conditions were similarly low in the two dietary groups. Fifteen minutes after endotoxin administration, PAF and lyso‐PAF contents increased significantly, and the PAF content in the high α‐linolenate group was 60% lower than in the high linoleate group; the lyso‐PAF contents also tended to be lower. Lyso‐PAF acetyltransferase and CoA‐independent transacylase activities in kidney microsomes increased significantly after endotoxin administration, while PAF acetylhydrolase activity in the cytosol was relatively unchanged. The lyso‐PAF acetyltransferase and PAF acetylhydrolase activities did not differ between the two dietary groups, but the CoA‐independent, transacylase activity was roughly 30% lower in the high α‐linolenate group. In agreement with in vitro study, our present study demonstrates that dietary high α‐linolenate suppresses PAF production in rat kidney during systemic endotoxemia, and which is mainly due to the decrease in alkylacyl‐GPC content, altered fatty acid compositions of the precursor lipids and lower CoA‐independent transacylase activity.