Insecticidal effects of extracts of seven plant species on larval development, alpha-amylase activity and offspring production of Tribolium castaneum (Herbst) (Insecta: Coleoptera: Tenebrionidae).

Bioinsecticidal effects of methanol extracts from seven plant species on Tribolium castaneum were investigated. Centaurium erythraea, Peganum harmala, Ajuga iva, Aristolochia baetica, Pteridium aquilinum and Raphanus raphanistrum extracts inhibit growth of larvae. C. erythraea was the most toxic with 63% mortality 10 days after treatment, followed by P. harmala with 58%. C. erythraea and P. aquilinum reduce the emergence rate respectively of 66% and 19%. The duration of larval period was shortened by Launaea arborescens, P. aquilinum and A. iva extracts, whereas R. raphanistrum and P. harmala extracts extend the larval period when compared to the control. Extracts of C. erythraea, P. harmala, A. iva and A. baetica inhibited F1 progeny production. Larvae possess three alpha-amylase isoforms as determined by SDS-PAGE. Larvae fed on treated diet had lower alpha-amylase activity than larvae feed on untreated diet. C. erythraea and P. harmala are the most potent extracts. These plant extracts could be useful to reduce seed damage caused by this pest species.

Endocrine and neuroendocrine effects of Azadirachtin in adult females of the earwig Labidura riparia.

In previous studies we have shown that injection of the insect growth regulator Azadirachtin (AZA) into young vitellogenic females induces inhibition of vitellogenesis in a dose-dependent manner. Juvenile hormone treatment rescues vitellogenin synthesis and ovarian growth. The cytopathological effects on ovaries and fat body are not linked to an inhibition of feeding. In this work we investigated the effects of AZA on the endocrine and neuroendocrine system. Enzyme immunoassay reveals that ovarian ecdysteroid levels are drastically reduced, in a dose-dependent fashion, by AZA. Ultrastructural study indicates that corpus allatum cells exhibit signs of inactivity and degenerative changes after AZA exposure. Using an antibody against allastostatin-3 of Blatella germanica (BLAST-3), we show the appearance of strong immunoreactivity of numerous cells and axons in the brain of AZA-injected females. We conclude that vitellogenesis inhibition by AZA consists of a direct cytotoxic effect as well as a generalized disruption of endocrine and neuroendocrine functions.

Effect of Azadirachtin on vitellogenesis of Labidura riparia (Insect Dermaptera).

This study investigates the effects of the insect growth regulator Azadirachtin (AZA) on the ultrastructure of ovaries and fat body of the earwig Labidura riparia. Ovarian development is severely reduced in AZA-injected females in a dose-dependent manner. Follicles exhibit degenerative changes, separation of follicle cells from the oocyte, and lack of pinocytotic vesicles as of yolk spheres in cortical ooplasm. Adipocytes show fragmented rough endoplasmic reticulum (RER), numerous autophagic vacuoles, multivesicular bodies, osmiophilic lipid droplets, and many large glycogen areas. Gel electrophoresis reveals that vitellogenin is absent from both fat body and hemolymph, and that vitellin is not deposited in the ovary. These pathological effects are not linked to an absence of feeding. The effect of AZA on vitellogenesis is rescuable by Juvenile hormone (JH) treatment. The inhibition of vitellogenesis by AZA is discussed on the basis of its direct cytotoxic effect as well as its interference with the neuroendocrine system.

In vivo inhibition of vitellogenesis in the Dermapteran Labidura riparia by 20-hydroxyecdysone.

In previous studies we have described the existence of cyclical changes in ecdysteroid levels during the female reproductive life of the earwig Labidura riparia. High levels of ecdysteroids are observed at the end of each vitellogenic period just before follicle degeneration, in coincidence with the beginning of each non-vitellogenic period. In the present work, using in vivo [(35)S]methionine incorporation, electrophoresis and electron microscopy, we study the effects on fat body and ovaries of 20-hydroxyecdysone (20E) injections into young vitellogenic females. This resulted in a reduction of proteosynthetic organelles (scarce Golgi complexes and fragmented RER cisternae), inhibition of vitellogenin synthesis in adipocytes, vitellogenesis arrest and premature follicular atresy. All these effects are suppressed when juvenile hormone treatment is associated with 20E injections. 20E does not inhibit vitellogenesis when applied to pars lateralis deprived females, which display continuous vitellogenesis. Thus, 20E does not act directly on ovaries nor on corpus allatum: the presence of the pars lateralis cells is required for 20E to inhibit vitellogenesis. These findings are explained in terms of the existence of a 20E feed back loop. This hormone acts via lateral neurosecretory cells of the brain which probably have an allatostatic effect.

Hormones regulating structural changes in the adipocytes of the female earwig Labidura riparia.

Changes in periovarian fat body fine structure occur during the reproductive cycle of the female earwig Labidura riparia. During the process of vitellogenesis, high levels of protein synthesis are seen in the adipocytes. Simultaneously, the formerly osmiophilic lipid droplets become non-osmiophilic, while an osmiophilic material diffuses from lipid droplets to the cisternae of the rough endoplasmic reticulum (RER). These structural features alter during non-vitellogenic periods: RER and Golgi apparatus regress and seem to be inactive. Lipid droplets are once again osmiophilic and no material enters into RER cisternae. Using microsurgical manipulations, hormonal treatments and light and electron microscopy, we have investigated the regulation of these changes. The neuroendocrine cerebral centre pars intercerebralis, by the action of the juvenile hormone of the corpus allatum. triggers protein metabolism. Another neuroendocrine center, the pars lateralis. and the hormone 20-hydroxyecdysone, regulate structural lipid droplet changes in the adipocytes.