bifenthrin and thiacloprid

The CncC pathway regulates the expression of multiple detoxification genes and contributes to the detoxification and antioxidation in insects. Many studies have focused on the impacts of plant allelochemicals on the CncC pathway, whereas studies on the effects of pesticides on key genes involved in this pathway are very limited. In this study, the effects of different types of commonly used insecticides on the transcripts of CncC, Keap1, and Maf and multiple detoxification genes of Helicoverpa armigera were evaluated using real-time quantitative polymerase chain reaction. The results showed that 8 insecticides (bifenthrin, λ-cyhalothrin, chlorantraniliprole, cyantraniliprole, spinosad, indoxacarb, chlorfenapyr, tolfenpyrad, and thiacloprid) significantly induced the expression of CncC and 4 insecticides (cypermethrin, acetamiprid, thiacloprid, and indoxacarb) suppressed the expression of Keap1 both at 24 h and 48 h; meanwhile, the expression levels of Maf were induced by 5 insecticides (fenvalerate, chlorantraniliprole, cyantraniliprole, lufenuron, and tolfenpyrad) at 24 h or 48 h. Multiple detoxification genes, especially cytochrome P450s genes, showed different up-regulation after bifenthrin, λ-cyhalothrin, chlorantraniliprole, cyantraniliprole, indoxacarb, and spinosad treatment for 48 h. Our results suggest that the CncC pathway and detoxification genes can be activated by different insecticides in H. armigera. These results establish a foundation for further studies on the relationship between the CncC pathway and the detoxification genes in H. armigera.

Topics: Animals; Insecticides; Kelch-Like ECH-Associated Protein 1; Moths; NF-E2-Related Factor 2

Pesticide toxicity may be modified by a number of co-occurring environmental and ecological stressors. Coexposure to predator cues has been shown to potentiate and/or synergize toxicity of pesticides. However, the mechanisms behind these interactions are not well understood. Here we examine the effects of fish predator (bluegill, Lepomis macrochirus) cues on toxicity of five different pesticides to the freshwater cladoceran, Ceriodaphnia dubia. The purpose for examining patterns among pesticides was to test the idea that the mechanism of the interaction could be explained by a general stress response; that is, the interaction patterns would be similar regardless of the pesticide's mechanism of action [MOA]). Acute 96-h concentration-response experiments were conducted for pesticides with and without fish cues. Predator cues influenced the toxicity of pesticides and the interaction patterns varied among pesticides. Fipronil exhibited a synergistic interaction, while predator cues interacted antagonistically for bifenthrin and thiacloprid. Other compounds previously reported to potentiate toxicity (malathion) were found to act additively. The results demonstrate that factors such as pesticide bioavailability, K(OC) , and exposure concentration may be important for predicting the occurrence of these interactions and that patterns were not consistent among pesticides varying in MOA. Predator stress is an important component for structuring communities and ecosystem processes. Fully understanding how this process may interact with organic contaminants may best be achieved by examination at toxicokinetic and toxicodynamic scales.

Topics: Animals; Cues; Daphnia; Drug Interactions; Ecosystem; Fresh Water; Malathion; Neonicotinoids; Perciformes; Pesticides; Pheromones; Predatory Behavior; Pyrazoles; Pyrethrins; Pyridines; Stress, Physiological; Thiazines; Water Pollutants, Chemical