Histopathological and cytotoxic changes induced by spinosad on midgut cells of the non-target predator Podisus nigrispinus Dallas (Heteroptera: Pentatomidae).

Broad-spectrum insecticides used in pest control are a risk for non-target insects. Their compatibility to the insecticide spinosad, used in agriculture and forestry as a biological control tool, needs to be evaluated. Podisus nigrispinus Dallas (Heteroptera: Pentatomidae) is a predatory bug used in the pest management of agricultural and forest systems where spinosad is also frequently applied. The aim of this study was to evaluate the toxicity, histopathology and cytotoxicity in midgut cells of P. nigrispinus exposed to spinosad. The toxicity test was performed to determine the lethal concentrations of spinosad after exposure by ingestion. The histopathology and cytotoxicity caused by spinosad were analyzed in the three midgut regions (anterior, middle and posterior) of P. nigrispinus during different exposure periods. Spinosad, at low concentrations, was toxic to P. nigrispinus [LC50 = 3.15 (3.02-3.26) µg.L-1]. Cell degeneration features such as cytoplasm vacuolization, chromatin condensation and release of cell fragments to the midgut lumen were observed in this organ. Cell death via apoptosis was found in the three midgut regions of this predator after exposure to the insecticide. Spinosad is toxic to P. nigrispinus, and causes histological and cytological damage followed by cell death in the midgut, suggesting a dangerous effect on a beneficial non-target insect.

Exposure to Insecticides Reduces Populations of Rhynchophorus palmarum in Oil Palm Plantations with Bud Rot Disease.

The South American palm weevil (SAPW), Rhynchophorus palmarum Linnaeus (Coleoptera: Curculionidae) is the main pest of Elaeis guineensis and damages palm trees with bud rot disease in the Americas. The effects of six neurotoxic insecticides (abamectin, carbaryl, deltamethrin, fipronil, imidacloprid and spinosad) were evaluated against SAPW for toxicity, survival, reproduction, and mortality. Abamectin (LC50 = 0.33 mg mL-1), Carbaryl (LC50 = 0.24 mg mL-1), deltamethrin (LC50 = 0.17 mg mL-1), and fipronil (LC50 = 0.42 mg mL-1) were the most toxic to SAPW. Adult survival was 95% without exposure to insecticides, decreasing to 78-65% in insects treated with the LC25 and 49-35% in insects exposed to LC50. Sublethal doses of carbaryl, fipronil and imidacloprid showed significant effect on the reproduction of this insect. Mortality of SAPW populations caused by insecticides had similar effects in the laboratory and field conditions. The results suggest that carbaryl, deltamethrin, fipronil, and imidacloprid caused significantly higher mortality as compared to the control in SAPW and may be used to control its populations in oil palm trees where bud rot appears as the key disease for SAPW attraction and infestation.

Exposure to spinosad induces histopathological and cytotoxic effects on the salivary complex of the non-target predator Podisus nigrispinus.

In integrated pest management systems, biological and chemical controls must be compatible. The insecticide spinosad affects some non-target insects and might compromise their fitness. The objective of this study was to evaluate the histopathological and cytotoxic effects of spinosad on the salivary complex of the predatory bug Podisus nigrispinus (Heteroptera: Pentatomidae). Spinosad toxicity and insect survival were determined using six concentrations of insecticide. Ultrastructural changes and cell death of salivary glands were analyzed after P. nigrispinus exposure to spinosad LC50 (3.15 µg L-1). The insecticide caused toxicity to P. nigrispinus; survival was 32% after 48 h of exposure to LC50. The main histological changes in the salivary complex were disorganization of the epithelium, cytoplasmic vacuolization, and apocrine secretion into the gland lumen. Cytotoxic effects, such as release of granules and vacuoles into the lumen, presence of autophagosomes, enlargement of basal plasma membrane infoldings, and apoptosis, were observed. Spinosad causes toxicity, decreases survival, and changes the histology and cytology of the P. nigrispinus salivary complex. The results suggest that the cellular stress induced by the insecticide affects extra-oral digestion, compromising the potential of P. nigrispinus as a biological pest control agent.