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 (2alpha,3alpha(OH)2-Delta22-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. RH 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 [3H]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.
Charrois
GJR
Department of Biological Sciences, University of Alberta, Edmonton, Alberta, T6G 2E9, Canada
Mao
H
Kaufman
WR