Pestic Biochem Physiol. 1996 Jun;55(2):140-9. doi: 10.1006/pest.1996.0043.
Impact on Salivary Gland Degeneration by Putative Ecdysteroid Antagonists and Agonists in the Ixodid Tick Amblyomma hebraeum.
Pesticide biochemistry and physiology
Charrois, Mao, Kaufman
Affiliations
Affiliations
- Department of Biological Sciences, University of Alberta, Edmonton, Alberta, T6G 2E9, Canada
PMID: 8980038
DOI: 10.1006/pest.1996.0043
Abstract
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 μg/ml, 8.4 μM) did not attenuate degeneration caused by 20-hydroxyecdysone; on the contrary, it enhanced the degree of salivary gland degeneration. SSBR (up to 4.5 μg/ml, 9 μM) likewise did not reduce 20-hydroxyecdysone mediated degeneration. RH 5849 up to 15 μg/ml (51 μM) and RH 5992 up to 10 μg/ml (28 μM) had no ecdysone-mimicking effect. In vivo, both RH compounds had an ecdysone-mimicking effect. RH 5849 (but not RH 5992) at 10 μg/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 μg/ml (12-14 μM) or below. RH 5849 (14 μg/ml, 47 μM) displaced 8% of (PoA) binding; at 68 μg/ml (230 μM) displacement was 30%. For RH 5992 inhibition of PoA binding was 16, 33, and 43% at 4.5, 16, and 79 μg/ml (13, 45, and 79 μM), 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.
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