Lethal and sublethal effects of toxic bait formulations on Doryctobracon areolatus (Hymenoptera: Braconidae) and implications for integrated fruit fly management.

The use of toxic baits has become one of the main methods of management of fruit flies in Brazil. The application of toxic baits may cause side effects on the native parasitoid Doryctobracon areolatus (Hymenoptera: Braconidae). Based on the results, formulations made from the food attractants 3% Biofruit, 1.5% Ceratrap, 1.25% Flyral, 3% Isca Samaritá, 3% Isca Samaritá Tradicional, and 7% sugarcane molasses associated with the Malathion 1000 EC and the ready-to-use toxic bait Gelsura (containing the active ingredient alpha-cypermethrin) were classified as harmful (class 4) to D. areolatus (mortality > 85% at 96 HAE). In contrast, for toxic baits formulated with insecticide phosmet, the mortality ranged from 38% to 72%, classified as slightly harmful or moderately harmful. However, when phosmet was added to the 3% Samaritá Tradicional bait, the mortality was only 3.9% (class 1-harmless), similar to the toxicity observed for the Success 0.02 CB ready-to-use bait (0.24 g a.i. spinosad/l) (<5% mortality). Although toxic baits were formulated with spinosyn-based insecticides, all toxic bait formulations were classified as harmless or slightly harmful (<50% mortality) to D. areolatus, with the exception of 1.5% Ceratrap + spinetoram and 7% Sugarcane molasses + spinosad (≈ 60% mortality-moderately harmful). In addition, these formulations did not show sublethal effects in reducing the parasitism and emergence rate of the F1 generation of D. areolatus in A. fraterculus larvae. The results serve as a basis for the correct use of toxic food baits without affecting the biological control.

The impact of six insecticides commonly used in control of agricultural pests on the generalist predator Hippodamia convergens (Coleoptera: Coccinellidae).

Hippodamia convergens is an important predator found in different agroecosystems. We evaluated the impacts of six insecticides on eggs, larvae and adults of this predator. For eggs, all insecticides reduced larval hatching rates, but did not affect egg duration. Chlorpyrifos and phosmet reduced larval survival; and chlorpyrifos, etofenprox and phosmet prolonged the larva development time. The survival and duration of pupae were not affected by all insecticides tested. Chlorpyrifos reduced fecundity, fertility and longevity when eggs were sprayed. For first-instar larvae, chlorpyrifos, etofenprox, phosmet and imidacloprid caused 100% mortality, while azadirachtin and thiamethoxam caused 35.0 and 52.7% mortality, respectively. However, azadirachtin and thiamethoxam did not affect the other biological parameters of the predator. In adults, chlorpyrifos, etofenprox and phosmet reduced adult survival. Chlorpyrifos, etofenprox, and phosmet reduced fecundity and longevity, but did not affect fertility. Azadirachtin, imidacloprid and thiamethoxam did not affect fecundity, fertility or longevity. Based on demographic parameters, all insecticides reduced the net reproductive rate (Ro), intrinsic rate of increase (r) and finite rate of increase (λ) of the predator when eggs were treated directly. Azadirachtin, chlorpyrifos, etofenprox and phosmet increased the mean generation time (T), while the effects of imidacloprid and thiamethoxam were similar to the control. When first-instar larvae were treated, azadirachtin and thiamethoxam reduced the Ro, r and λ. Thiamethoxam increased the T value, while the effects of the other insecticides were similar to the control. These insecticides should be used with caution, in order to reduce their harmful effects on the predator in agroecosystems.

Effects of the organophosphate insecticides phosmet and chlorpyrifos on trophoblast JEG-3 cell death, proliferation and inflammatory molecule production.

Epidemiological data have associated environmental organophosphate insecticide (OP) exposure during pregnancy with fetal growth deficits. To better understand OP injury that may adversely affect pregnancy, we used the JEG-3 choriocarcinoma cell line, which provide a recognized in vitro model to study placental function. The effects of the OP phosmet (Pm) and chlorpyrifos (Cp) on JEG-3 cells viability, proliferation, cell cycle and inflammatory molecule production were evaluated. Both insecticides affected cellular viability in a concentration- and time-dependent manner, inducing apoptosis and decreasing [(3)H]-thymidine incorporation. However, only Pm reduced DNA synthesis independently of cellular death and decreased the cell percentage at the S-phase. Unlike apoptosis, TNFα production varied with the concentration tested, suggesting that other TNFα independent mechanisms might trigger cell death. No induction of the inflammatory molecule nitric oxide was detected. The mRNA levels of pro-inflammatory IL-6, IL-17 and the anti-inflammatory IL-13 cytokines were differentially modulated. These findings show that Pm and Cp generate a specific toxicity signature, altering cell viability and inducing an inflammatory cytokine profile, suggesting that trophoblasts may represent a possible target for OP adverse effects.

Phosphoinositide phosphorylation and shape changes produced by phosmet-oxon in human erythrocytes.

1. "In vitro" incubation of red blood cells with phosmetoxon induced crenated and invaginated forms. 2. [32P] phosphate incorporation was greater in membranes from erythrocytes exposed to 300 nM phosmetoxon for 10 min than in control cells. 3. The highest incorporation was for phosphatidylinositol (PI), followed by phosphatidylinositol phosphate (PIP) and phosphatidylinositolbiphosphate (PIP2). 4. An activation of phosphatidylinositol (PI) kinase was detected with 150 and 300 nM of the pesticide, while there was no change in poliphosphoinositides (PPI) phosphodiesterase activity. 5. Results suggest an association between changes in PI kinase activity, the phosphorylation cycle of phosphatidylinositols and alterations in erythrocyte morphology induced by phosmetoxon.