Release of leukotriene C<sub>4</sub> from human polymorphonuclear leucocytes as determined by radioimmunoassay

Aehringhaus, U.; Wölbling, R.H.; König, Wolfgang; Patrono, Carlo; Peskar, B. M.

doi:10.1016/0014-5793(82)80715-1

Cited by 114 publications

(43 citation statements)

References 24 publications

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“…The recovery of the PGE2 internal standard was 60-70%. Methanol fraction was also evaporated, and the dried residue was used for RIA with an LTC4 3H-RIA kit (34). The recovery of the LTC4 internal standard in the final sample was 75-80%.…”

Section: Extraction and Radioimmunoassay Ofpge2 And Ltc4mentioning

confidence: 99%

Stimulated arachidonate metabolism during foam cell transformation of mouse peritoneal macrophages with oxidized low density lipoprotein.

Yokode¹,

Kita²,

Kikawa³

et al. 1988

J. Clin. Invest.

155

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Changes in arachidonate metabolism were examined in mouse peritoneal macrophages incubated with tarious types of lipoproteins. Oxidized low density lipoprotein (LDL) was incorporated by macrophages and stimulated macrophage prostaglandin E2 (PGE2) and leukotriene C4 syntheses, respectively, 10.8-and 10.7-fold higher than by the control. Production of 6-keto-PGFI,, a stable metabolite of prostacyclin, was also stimulated. No stimulation was found with native LDI, which was minimally incorporated by the cells. Acetylated LDL and beta-migrating very low density lipoprotein (Ol-VLDL), though incorporated more efficiently than oxidized LDL, also had no stimulatory effect. When oxidized LDL was separated into the lipoprotein-lipid peroxide complex and free lipid peroxides, most of the stimulatory activity was found in the former fraction, indicating that stimulation of arachidonate metabolism in the cell is associated with uptake of the lipoprotein-lipid peroxide complex. These results suggest that peroxidative modification of LDL could contribute to the progression of atheroma by stimulating arachidonate metabolism during incorporation into macrophages.

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Section: Extraction and Radioimmunoassay Ofpge2 And Ltc4mentioning

confidence: 99%

Stimulated arachidonate metabolism during foam cell transformation of mouse peritoneal macrophages with oxidized low density lipoprotein.

Yokode¹,

Kita²,

Kikawa³

et al. 1988

J. Clin. Invest.

155

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“…Cross-reactivities have previously been determined for anti-sera to LTB4 (Salmon et al, 1982), LTC4 (Aehringhaus et al, 1982) 6-keto-PGFl, and TXB2 (Salmon, 1978). The anti-sera to LTC4 cross-reacts by up to 40% with LTD4 (Aehringhaus et al, 1982).…”

Section: Radioimmunoassaymentioning

confidence: 99%

Failure of the inhibition of rat gastric mucosal 5‐lipoxygenase by novel acetohydroxamic acids to prevent ethanol‐induced damage

Boughton‐Smith

Whittle

1988

British J Pharmacology

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The role of leukotriene B4 (LTB4) and LTC4 as mediators of gastric mucosal damage following ethanol challenge in vivo has been investigated using two selective 5‐lipoxygenase inhibitors, BW A4C and BW A137C. Oral administration of ethanol to rats in vivo, induced macroscopic damage to the gastric mucosa and markedly increased the formation of the 5‐lipoxygenase products, LTB4 and LTC4, from the mucosa ex vivo. Pretreatment with the acetohydroxamic acids BW A4C and BW A137C (5–50 mg kg−1 p.o.) dose‐dependently reduced ethanol‐stimulated LTB4 and LTC4 formation by the gastric mucosa, with an ID50 of approximately 5 mg kg−1 p.o. A single oral dose of BW A4C (20 mg kg−1) induced near‐maximal inhibition of mucosal LTB4 formation within 30 min, which was well maintained for 5h, whereas BW A137C (20 mg kg−1 p.o.) induced maximal inhibition between 30 and 60 min after administration, which then diminished over the subsequent 5 h. The mucosal formation of the cyclo‐oxygenase product, 6‐keto‐prostaglandin F1α, which was unaltered following ethanol challenge, was not inhibited by the acetohydroxamic acids. Likewise, the small increase in mucosal thromboxane B2 formation following challenge was not inhibited by BW A4C. Neither BW A4C nor BW A137C, at doses that almost completely inhibited the mucosal synthesis of LTB4 or LTC4, reduced the macroscopic gastric mucosal damage induced by ethanol. Pretreatment with the lipoxygenase inhibitor BW 755C (5–50 mg kg−1 p.o.) did reduce mucosal damage, but there was a dissociation between the degree of protection and the inhibition of leukotriene biosynthesis. Oral administration of high doses of either BW A4C or BW A137C (300 mg kg−1) did not induce macroscopic gastric damage over a 3 h period. These findings suggest that the leukotrienes, LTB4 and LTC4 are not the primary mediators of ethanol‐induced acute mucosal damage, but do not exclude their role in more chronic gastric damage and inflammation.

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“…The specificity of the antisera used in these RIAs has been previously established: TXB2, 6-oxo-PGF 1. and PGE2 (Salmon, 1978), LTB4 (Salmon et al, 1982) and LTC4 (Aehringhaus et al, 1982 (Sigma). FPL 55712 (sodium 7-(3(4-acetyl-3-hydroxy-2-propylphenoxy)-2-hydroxy-propoxy)-4-oxo-8-propyl-4H-I -benzopyran-2-carboxylate) was a gift from Fisons Ltd, Loughborough; U-46619…”

Section: Radioimmunoassay Of the Lung Effluentmentioning

confidence: 99%

Differential release of eicosanoids by bradykinin, arachidonic acid and calcium ionophore A23187 in guinea‐pig isolated perfused lung

Bakhle

Moncada

Nucci³

et al. 1985

British J Pharmacology

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IThe effects of infusions of bradykinin (0.2 fLM), calcium ionophore A23 187 (0.5 LM) and arachidonic acid (13 LM) on the release of eicosanoids from the guinea-pig isolated perfused lung were investigated using radioimmunoassay for thromboxane B2 (TXB2), 6-oxo-prostaglandin Flm (6-oxo-PGF,.), PGE2, leukotriene B4 (LTB4) and LTC4 and bioassay using the superfusion cascade. 2 Bradykinin released more 6-oxo-PGF,, than TXB2, whereas arachidonic acid and ionophore released more TXB2 than 6-oxo-PGF,,.3 The time course of eicosanoid release varied with the stimulus: bradykinin and arachidonic acid produced an immediate release, whereas the ionophore showed a slower onset of release. 4 Although the amounts of LTB4 and LTC4 released by the ionophore were very low according to radioimmunoassays, there was evidence from the bioassay of release of a leukotriene-like substance, thought to be LTD4. 5 The leukotriene antagonist FPL 55712 lacks specificity in the guinea-pig trachea; at the concentration used (2 tiM) it antagonized contractions of the tracheal strip to PGE2 as well as to LTC4. 6 Our results show that in the guinea-pig perfused lung the metabolism of exogenous arachidonic acid is both qualitatively and quantitatively different from the metabolism of endogenous arachidonic acid; furthermore, the profile of eicosanoid production is stimulus-dependent.

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Release of leukotriene C₄ from human polymorphonuclear leucocytes as determined by radioimmunoassay

Cited by 114 publications

References 24 publications

Stimulated arachidonate metabolism during foam cell transformation of mouse peritoneal macrophages with oxidized low density lipoprotein.

Stimulated arachidonate metabolism during foam cell transformation of mouse peritoneal macrophages with oxidized low density lipoprotein.

Failure of the inhibition of rat gastric mucosal 5‐lipoxygenase by novel acetohydroxamic acids to prevent ethanol‐induced damage

Differential release of eicosanoids by bradykinin, arachidonic acid and calcium ionophore A23187 in guinea‐pig isolated perfused lung

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Release of leukotriene C4 from human polymorphonuclear leucocytes as determined by radioimmunoassay

Cited by 114 publications

References 24 publications

Stimulated arachidonate metabolism during foam cell transformation of mouse peritoneal macrophages with oxidized low density lipoprotein.

Stimulated arachidonate metabolism during foam cell transformation of mouse peritoneal macrophages with oxidized low density lipoprotein.

Failure of the inhibition of rat gastric mucosal 5‐lipoxygenase by novel acetohydroxamic acids to prevent ethanol‐induced damage

Differential release of eicosanoids by bradykinin, arachidonic acid and calcium ionophore A23187 in guinea‐pig isolated perfused lung

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Release of leukotriene C₄ from human polymorphonuclear leucocytes as determined by radioimmunoassay