Impact on salivary gland degeneration by putative ecdysteroid antagonists and agonists in the ixodid tick Amblyomma hebraeum

Ecdysteroids cause salivary gland degeneration in female ixodid ticks. We tested the effects of the following compounds on salivary gland degeneration in the ixodid tick Amblyomma hebraeum Koch: HHCS (22S,23S-homocastasterone), SSBR (22S,23S-homobrassinolide), STGM (2 alpha,3 alpha(OH)(2)-Delta(22)-stigmasten-6-one), RH 5849, and RH 5992. The first three are brassinosteroids (putative ecdysone antagonists) and the last two are nonsteroidal mimics of ecdysone in a variety of insects. In vitro, HHCS (up to 4 mu g/ml, 8.4 mu M) did not attenuate degeneration caused by 20-hydroxyecdysone; on the contrary, it enhanced the degree of salivary gland degeneration. SSBR (up to 4.5 mu g/ml, 9 mu M) likewise did not reduce 20-hydroxyecdysone mediated degeneration. RW 5849 up to 15 mu g/ml (51 mu M) and RH 5992 up to 10 mu g/ml (28 mu M) had no ecdysone-mimicking effect. In vivo, both RH compounds had an ecdysone-mimicking effect. RH 5849 (but not RH 5992) at 10 mu g/tick increased ovary wet weight slightly. None of the brassinosteroids displaced a significant amount of [H-3]ponasterone A (PoA) from the ecdysone receptor at 6 mu g/ml (12-14 mu M) or below. RH 5849 (14 mu g/ml, 47 mu M) displaced 8% of (PoA) binding; at 68 mu g/ml (230 mu M) displacement was 30%. For RH 5992 inhibition of PoA binding was 16, 33, and 43% at 4.5, 16, and 79 mu g/ml (13, 45, and 79 mu M), respectively. Overall, the brassinosteroids and the RH compounds do not act on the tick salivary gland ecdysteroid system in a way similar to the Way they act on some insect systems. (C) 1996 Academic Press, Inc.