Research Article| Volume 13, ISSUE 2, P211-216, February 1984

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

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      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 1-histidine dose dependently. In the same way 1-histidine diminished the aggregation-induced synthesis of TXB2 in human platelets. In contrast to this, after incubation with 1-histidine the generation of PGE2 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 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.
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        • Borden A.L.
        • Wallraff E.B.
        • Brodie E.C.
        • Holbrook W.P.
        • Hill D.F.
        • Stephens C.A.L.
        • Kent L.J.
        • Kemmerer A.R.
        Plasma levels of free amino acids in normal subjects compared with patients with rheumatoid arthritis.
        in: Proc. Soc. Exp. Biol. Med.75. 1950: 28
        • Nettelbladt E.
        • Sandell B.
        Amino-acid content of serum in rheumatoid arthritis.
        Ann. Rheum. Dis. 1963; 22: 269
        • Gerber D.A.
        Low free serum histidine concentration in rheumatoid arthritis. A measurement of disease activity.
        J. Clin. Invest. 1975; 55: 1164
        • Brückner-Schmidt R.
        • Jackisch R.
        • Hertting G.
        Stimulation of PGE2-synthesis by noradrenaline in primary rabbit splenic pulpa is mediated by atypical a-adrenoceptors.
        Naunyn-Schmiedeberg's Arch. Pharmacol. 1981; 316: 1
        • Born G.V.R.
        Quantitative investigations into the aggregation of blood platelets.
        J. Physiology (London). 1962; 162: 67P
        • Dray F.
        • Charbonnel B.
        • Maclouf J.
        Radioimmunoassay of prostaglandin Fα, E1 et E2 in human plasma.
        Europ. J. Clin. Invest. 1975; 5: 311
        • Steinhauer H.B.
        • Hertting G.
        Lowering of the convulsive threshold by non-steroidal anti-inflammatory drugs.
        Europ. J. Pharmacol. 1981; 69: 199
        • Steinhauer H.B.
        • Lubrich I.
        • Günter B.
        • Schollmeyer P.
        Response of human platelets to inhibition of thromboxane synthesis.
        Clin. Hemorheology. 1983; 3: 1
        • Needleman P.
        • Bryan B.
        • Wyche A.
        • Bronson S.D.
        • Eakins K
        • Ferrendelli J.A.
        • Minkes M.
        Thromboxane synthetase inhibitors as pharmacological tools: Differential biochemical and biological effects on platelet suspensions.
        Prostaglandins. 1977; 14: 897
        • Anhut H.
        • Jackisch R.
        • Peskar B.A.
        Thromboxane B2 release and H-noradrenaline accumulation by a synaptosomal fraction of rat brain.
        Pol. J. Pharmacol. Pharm. 1979; 31: 381
        • Steinhauer H.B.
        • Anhut H.
        • Hertting G.
        Inhibition of thromboxane synthesis in mouse brain in vivo.
        Naunyn-Schmiedeberg's Arch. Pharmacol. 1980; 311: R117
        • Gerber D.A.
        • Pinals R.S.
        Mechanism by which hypohistidinemia could contribute to the pathogenesis of rheumatoid arthritis.
        in: Partsch G. Batsford S. Histidine. II. Georg Thieme-Verlag, Stuttgart, New York1980: 12