Abstract

JH levels in Manduca sexta larvae were suppressed in a dose dependent fashion following topical treatment with either the potent juvenoids fenoxycarb or hydroprene, or the anti juvenile hormone (AJH) agent (3R,S)- fluoromevalonolactone (FMev>). We determined ED 50 values, expressed as the amount of substance (applied topically to early third stadium larvae) required to lower JH titer (determined in the early fourth stadium) by 50%; these values were 0.001, 0.1 and 3 μg for fenoxycarb, hydroprene, and FMev>, respectively. Combined enzymatic and chemical methods were used to prepare a sample containing predominatly (−)FMev>. Comparison of dose-response curves obtained following treatment of M. sexta larvae with (−)FMev>;, versus treatment with racemic FMev>f, confirmed that the (−)enantiomer is the active principle. Similarly, we showed that the (−)optical isomer of the “mixed” JH agonist/antagonist ethyl 4-[2-(t- butylcarbonyloxy) butoxy] benzoate (ETB) is the active principle of the racemic mixture. Injection or topical application of several intermediates of JH biosynthesis (mevalonlactone, homomevalonolactone or farnesoic acid) had little effect on resultant JH titer profiles in M. sexta larvae.

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