Abstract
The effects of chloroquine and mepacrine were determined on the release of slow reacting substances (leukotrienes) from lung fragments in vitro. These drugs have been shown in a variety of tissues to inhibit phospholipase A 2, and thus to reduce the availability of arachidonate, which is a substrate for leukotriene biosynthesis. Leukotriene and histamine release from unsensitized human lung was stimulated by calcium ionophore A23187, and from actively sensitized guinea-pig lung, by ovalbumin. Chloroquine (10 μM and 100 μM) significantly inhibited leukotriene release in lung from both species, and at 100 μM also inhibited histamine release. Mepacrine (10 μM) inhibited leukotriene release in human lung and at 100 μM in guinea-pig lung. The effects of chloroquine (100 μM) on leukotriene release were counteracted by the presence of arachidonic acid (10 μM), which suggests that chloroquine had impaired the availability of arachidonate. It seems probable that chloroquine and mepacrine inhibit leukotriene release by inhibition of phospholipase A 2 in lung.
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