Article date: June 1982
By: P.G. HELLEWELL, J.D. PEARSON in Volume 76, Issue 2, pages 319-326
The metabolism of prostaglandin F2α (PGF2α) 15 nM in 100,000 g supernatant fractions from piglet lung homogenates was inhibited by sulphasalazine with an IC50 value of 25 μm.
The piglet isolated lung perfused with Krebs solution, containing either albumin or Ficoll 70 to prevent oedema and vascular damage, efficiently metabolized PGF2α given as a bolus injection (1 ng in 0.1 ml; 30 nM).
In Krebs solution containing Ficoll 70, sulphasalazine inhibited the pulmonary inactivation of PGF2α in a dose‐dependent manner with an IC50 value of 110 μm. No inhibition of inactivation by sulphasalazine was found when the perfusion fluid contained albumin, which is known to bind this drug effectively.
Analysis of the separated efflux profiles for PGF2α and its metabolites with reference to the dilution curve for an extracellular marker provided evidence that sulphasalazine inhibited PGF2α uptake into lung cells.
We conclude that the effect of sulphasalazine on pulmonary prostaglandin inactivation is primarily due to inhibition of prostaglandin transport, and not to inhibition of prostaglandin metabolism.
The metabolism of prostaglandin F2α (PGF2α) 15 nM in 100,000 g supernatant fractions from piglet lung homogenates was inhibited by sulphasalazine with an IC50 value of 25 μm.
The piglet isolated lung perfused with Krebs solution, containing either albumin or Ficoll 70 to prevent oedema and vascular damage, efficiently metabolized PGF2α given as a bolus injection (1 ng in 0.1 ml; 30 nM).
In Krebs solution containing Ficoll 70, sulphasalazine inhibited the pulmonary inactivation of PGF2α in a dose‐dependent manner with an IC50 value of 110 μm. No inhibition of inactivation by sulphasalazine was found when the perfusion fluid contained albumin, which is known to bind this drug effectively.
Analysis of the separated efflux profiles for PGF2α and its metabolites with reference to the dilution curve for an extracellular marker provided evidence that sulphasalazine inhibited PGF2α uptake into lung cells.
We conclude that the effect of sulphasalazine on pulmonary prostaglandin inactivation is primarily due to inhibition of prostaglandin transport, and not to inhibition of prostaglandin metabolism.
DOI: 10.1111/j.1476-5381.1982.tb09223.x
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