The constant use of chemical insecticides for Aedes aegypti control has caused resistance in the mosquito populations. Thus, the objective of this study was to analyze the larvicidal potential of extracts and fractions of plants on A. aegypti larvae. The analysis included sixty one extracts and twenty five fractions of fifty botanical species at concentrations of 0.25; 0.12; 0.06 to 0.03 mg mL -1 ; 4 replications and one negative control of dechlorinate water and 1% DMSO; and a positive control with rotenone. The toxicity index in descending order with LC 50 for the most active of the extracts selected were ethanol extract of Ormosea arborea (0.111 mg mL -1 ) seeds and ethanol extracts of leaves such as Piper hispidum (0.169 mg mL -1 ),Solanum variabile (0.188 mg mL -1 ), O. arborea (0.238 mg mL -1 ), Turnera umifolia (0.242 mg mL -1 ) andPiper hispidum (0.567 mg mL -1 ). For plant fractions, the most active were chloroform (0.192 mg mL -1 ) and hexane (0.342 mg mL -1 ) P. aduncum leaves, hexane fraction (0.415 mg mL -1 ) and methanol extract (0.625 mg mL -1 ) of Spermacocea latifolia leaves. Regarding the extract of T. umifolia single species, there is no bibliographic report on their degree of efficiency as an insecticide.
Introduction: Dengue fever is a viral disease transmitted by the Aedes aegypti Linn. (1792) (Diptera: Culicidae) mosquito, which is endemic in several regions of Brazil. Alternative methods for the control of the vector include botanical insecticides, which offer advantages such as lower environmental contamination levels and less likelihood of resistant populations. Thus, in this study, the ability of botanical insecticide formulations to inhibit the activity of the liver enzymes serum cholinesterase and malate dehydrogenase was evaluated. Methods: Inhibition profi les were assessed using in vitro assays for cholinesterase and malate dehydrogenase activity and quantitated by ultraviolet-visible spectroscopy at 410nm to 340nm. Results: Insecticide products formulated from cashew nutshell liquid [A] and ricinoleic acid [B] showed cholinesterase activity levels of 6.26IU/mL and 6.61IU/mL, respectively, while the control level for cholinesterase was 5-12IU/mL. The products did not affect the level of 0.44IU/mL established for malate dehydrogenase, as the levels produced by [A] and [B] were 0.43IU/mL and 0.45IU/mL, respectively. Conclusions: Our fi ndings show that in vitro testing of the formulated products at concentrations lethal to A. aegypti did not affect the activity of cholinesterase and malate dehydrogenase, indicating the safety of these products.
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