Modification of prostaglandin generation by l-histidine — possible pathogenetic implication in rheumatoid arthritis

Abstract The effect of l-histidine on arachidonic acid metabolism was studied in rabbit splenic fibroblast cultures and human platelets. The noradrenaline-stimulated generation of PGE 2 in fibroblast cultures was inhibited by 1-histidine dose dependently. In the same way 1-histidine diminished the aggregation-induced synthesis of TXB 2 in human platelets. In contrast to this, after incubation with 1-histidine the generation of PGE 2 in activated platelets increased in a dose dependent way up to 240% of pretreatment values. The further increase of 1-histidine concentration resulted in an inhibition of platelet PGE 2 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.