Potencial Toxicogenético de inseticidas neonicotinóides em diferentes sistemas in vivo

Abstract

Thiamethoxam (TMX), Imidacloprid (IMI) and Acetamiprid (ACP) are defined as neonicotinoid neurotoxic insecticides, acting as agonists to nicotinic acetylcholine receptors. Actara® (AC), Premier® (PRM) and Mospilan® (MOP) are formulated products composed of TMX, IMI and ACP, respectively. The present study aimed to assess the toxicity and mutagenic, recombinogenic and carcinogenic potential of these insecticides. The mutagenic and recombinogenic effects were evaluated in vivo through the somatic mutation and recombination test (SMART) in Drosophila melanogaster. Larvae of 72h resulting from descendants of standard crosses (ST) and high metabolic bioactivation (HB) crosses were treated with different concentrations of TMX, IMI, ACP, AC, PRM or MOP for approximately 48 h. All the insecticides were toxic at the highest concentrations. TMX and AC were non-mutagenic at the ST crossing, but induced statistically significant increases in mutant spot frequencies at the concentrations of 9.7x10-4 and 1.9x10-3 mM regarding the HB crossing. IMI induced a significant increase only in those treated with 2.4 and 4.8x10-4 mM of the HB crossing, whereas the formulated PRM was mutagenic at all concentrations (from 1.2 to 9.7x10-4 mM) in both the crosses. ACP and MOP were not mutagenic considering the ST crossing. At the HB crossing, ACP induced a significant increase of mutant spots at all concentrations tested, while MOP was mutagenic only at the concentrations 1.9 and 3.9x10-3. The carcinogenic effects of insecticides were evaluated using the Epithelial Tumor Test (wts) in D. melanogaster. Larvae of 72h descended from the crossing between virgin females wts/TM3, Sb1 and mwh/mwh males were treated with the same concentrations used in SMART. In this case, carcinogenic activity was observed only in those treated with the PRM insecticide. As conclusion, the findings revealed toxic and mutagenic effects of the insecticides and their formulated products after being activated by cytochrome P450 enzymes (CYP6A2) (except PRM, which was mutagenic even at basal enzyme levels) and non-carcinogenic (except PRM, which showed carcinogenic effects). Thus, the inert ingredients interfere on the toxicity and mutagenicity of the active ingredients.