Quantum dots (QDs) hold promise for several biomedical, life sciences and photovoltaic applications. Substantial production volumes and environmental release are anticipated. QD toxicity may be intrinsic to their physicochemical properties, or result from the release of toxic components during breakdown. We hypothesized that developing zebrafish could be used to identify and distinguish these different types of toxicity. Embryos were exposed to aqueous suspensions of CdSe core / ZnS shell QDs functionalized with either poly-L-lysine or poly(ethylene glycol) terminated with methoxy, carboxylate, or amine groups. Toxicity was influenced by the QD coating, which also contributed to the QD suspension stability. At sublethal concentrations, many QD preparations produced characteristic signs of Cd toxicity that weakly correlated with metallothionein expression, indicating that QDs are only slightly degraded in vivo. QDs also produced distinctly different toxicity that could not be explained by Cd release. Using the zebrafish model, we were able to distinguish toxicity intrinsic to QDs from that caused by released metal ions. We conclude that developing zebrafish provide a rapid, low-cost approach for assessing structure-toxicity relationships of nanoparticles.
Injection of the insect growth regulator (IGR) azadirachtin into Manduca sexta larvae that were parasitized by Cotesia congregata adversely affected subsequent endoparasite development when the compound was administered prior to the first larval ecdysis of the wasps. Injection of 2.5–10 μg of azadirachtin into newly ecdysed fourth or fifth instar hosts partially inhibited or totally suppressed the first larval ecdysis of the parasites. Instead of initiating rapid growth similar to parasites developing in hosts injected with the solvent carrier (ethanol) only, parasites in azadirachtin‐treated hosts never grew beyond the size normally attained in early terminal stage hosts. The host larvae survived for 2 weeks or longer following injection of azadirachtin, but their parasites never recovered and died encased within one or two exuvial cuticles. The parasitism‐specific hemolymph polypeptides previously shown to be characteristic of terminal stage hosts were undetectable in larvae in which the parasites failed to ecdyse to the second instar. The observed effects of azadirachtin on development of C. congregata differ significantly from those induced by other IGRs in parasitized M. sexta, suggesting azadirachtin has a unique, though as yet undefined, mode of action. Compared to other IGRs, this compound is extremely potent in terms of the minimum doses required to prevent emergence, but affects only the L1‐L2 ecdysis and not the L2‐L3 transition. In contrast, other compounds such as juvenoids and the JH esterase inhibitor BEPAT (S‐benzyl‐0‐ethyl phosphoramidothiolate) permit the parasite to grow and develop normally until the wasps become pharate third instar larvae, then inhibit the second larval ecdysis and emergence from the host.
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