thromboxane-a2 and Taeniasis

The larval stage of the tapeworm, Taenia taeniaeformis, was incubated in different concentrations of arachidonic acid. At various times after incubation, aliquots were removed for bioassay on either 38 microM aspirin or non-aspirin-treated equine platelets and by radioimmunoassay for the thromboxane A2 breakdown product, thromboxane B2 (TXB2). Platelet agonist activity was detected as early as 30 sec after addition of the arachidonic acid. In aspirin-treated platelets, this agonist activity peaked at 1 to 4 min and thereafter decayed rapidly with a time course that was both worm and arachidonic acid dependent. When assayed on non-aspirin-treated platelets the agonist activity was again detectable as early as 30 sec after addition of arachidonic acid, peaked at 1 to 3 min and then decayed very slowly over a 30-min period of incubation. It was found that levels of TXB2 were detected which increased over time concomitant with the decay of the platelet agonist activity. The most consistent detection of TXB2 generation was at 30 min with a mean of 49.6 pg and a range of 22.1 to 84.8 pg for four experiments. This report presents the first evidence for arachidonic acid utilization by a cestode or trematode and could in part provide an explanation for the marked cellular inflammation noted around dead or dying parasites.

Topics: Animals; Arachidonic Acid; Arachidonic Acids; Aspirin; Horses; Imidazoles; Indomethacin; Kinetics; Larva; Platelet Aggregation; Rats; Taeniasis; Thromboxane A2; Thromboxane B2; Thromboxanes