Fenoxycarb, a potent contaminant of the silkworm, Bombyx mori L., does notinfluence its juvenile hormone titer

Citation
H. Monconduit et B. Mauchamp, Fenoxycarb, a potent contaminant of the silkworm, Bombyx mori L., does notinfluence its juvenile hormone titer, ARCH INS B, 40(3), 1999, pp. 141-149
Citations number
33
Categorie Soggetti
Entomology/Pest Control","Biochemistry & Biophysics
Journal title
ARCHIVES OF INSECT BIOCHEMISTRY AND PHYSIOLOGY
ISSN journal
07394462 → ACNP
Volume
40
Issue
3
Year of publication
1999
Pages
141 - 149
Database
ISI
SICI code
0739-4462(1999)40:3<141:FAPCOT>2.0.ZU;2-1
Abstract
Fenoxycarb (FC) effects were studied on juvenile hormone (JH) titers and JH -esterase activities in the silkworm, B. mori. In the literature, FC was ob served to induce high JH titers but also to act without corpora allata (CA) . These contradictory results did not permit us to conclude whether FC was a potent JH mimic or it was acting through the enhancement of JH titers in the hemolymph. Analysis of hemolymph JH-esterase activities during the last larval instar reveals that FC was not a JH-esterase inhibitor. Considering JHs, only JH II was detected in the European hybrid 200x300. Furthermore, JH titer was exactly identical in control and FC-treated larvae, i.e., it d ropped during the first 2 days of the last larval instar and became undetec table after day 2. This result is important since it contradicts the genera lly admitted concept that FC was acting by increasing the titer of JH. On t he contrary, it was found that, despite its non-terpenoid chemical structur e, FC might be a JH mimic. In addition, FC suspected contamination of mulberry leaves was analyzed fro m a physiological viewpoint, me observed that "contaminated" mulberry leave s-fed larvae became permanent larvae through the inhibition of their protho racic glands (PC;) activity and without any modification of their JH titers , i.e., exactly as for FC-treated larvae. This last point adds information concerning the suspected implication of FC in the induction of the non-spin ning syndrome. (C) 1999 Wiley-Liss, Inc.