Dietary alpha-linolenate suppresses endotoxin-induced platelet-activating factor production in rat kidney.
In comparison with dietary high-linoleate safflower oil, high alpha-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 alpha-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 alpha-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 alpha-linolenate group. In agreement with in vitro study, our present study demonstrates that dietary high alpha-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.
Oh-hashi
K
K
Department of Biological Chemistry, Faculty of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan.
Takahashi
T
T
Tanabe
A
A
Watanabe
S
S
Okuyama
H
H
D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase; D000123:Acetyltransferases / Q000187:drug effects / Q000378:metabolism; D000217:Acyltransferases / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D004041:Dietary Fats / Q000494:pharmacology*; D019446:Endotoxemia / Q000378:metabolism; D004731:Endotoxins / Q000494:pharmacology*; D005227:Fatty Acids / Q000032:analysis; D007668:Kidney / Q000187:drug effects / Q000378:metabolism*; D019787:Linoleic Acid / Q000494:pharmacology; D008297:Male; D010741:Phospholipases A / Q000187:drug effects / Q000378:metabolism; D010743:Phospholipids / Q000737:chemistry / Q000378:metabolism; D010972:Platelet Activating Factor / Q000096:biosynthesis*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017962:alpha-Linolenic Acid / Q000494:pharmacology*
D004041:Dietary Fats; D004731:Endotoxins; D005227:Fatty Acids; D010743:Phospholipids; D010972:Platelet Activating Factor; D017962:alpha-Linolenic Acid; D019787:Linoleic Acid; D000217:Acyltransferases; D000123:Acetyltransferases; C039766:arachidonyl transacylase; C046035:1-alkylglycerophosphocholine acetyltransferase; D010741:Phospholipases A; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase