Modification of prostaglandin generation by L-histidine--possible pathogenetic implication in rheumatoid arthritis.
The effect of l-histidine on arachidonic acid metabolism was studied in rabbit splenic fibroblast cultures and human platelets. The noradrenaline-stimulated generation of PGE2 in fibroblast cultures was inhibited by l-histidine dose dependently. In the same way l-histidine diminished the aggregation-induced synthesis of TXB2 in human platelets. In contrast to this, after incubation with l-histidine the generation of PGE2 in activated platelets increased in a dose dependent way up to 240% of pretreatment values. The further increase of l-histidine concentration resulted in an inhibition of platelet PGE2 synthesis. The present results demonstrate a differential influence of the amino acid l-histidine on cell arachidonic acid metabolism. It is concluded that the supposed anti-rheumatic property of l-histidine is caused by its effect on the synthesis of prostaglandins which are known to be mediators of inflammation.
D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism*; D001172:Arthritis, Rheumatoid / Q000503:physiopathology; D001792:Blood Platelets / Q000378:metabolism; D002478:Cells, Cultured; D015232:Dinoprostone; D006639:Histidine / Q000494:pharmacology*; D009638:Norepinephrine / Q000494:pharmacology; D011458:Prostaglandins E / Q000096:biosynthesis; D011817:Rabbits; D013154:Spleen / Q000378:metabolism; D013929:Thromboxane B2 / Q000096:biosynthesis
D001095:Arachidonic Acids; D011458:Prostaglandins E; D016718:Arachidonic Acid; D006639:Histidine; D013929:Thromboxane B2; D015232:Dinoprostone; D009638:Norepinephrine