Abstract
In this study, cypermethrin toxicity was investigated using physiological, biochemical and cytogenetic parameters, and more than one organ and cell type was preferred to determine these effects. In this multifaceted study, the genotoxicity mechanism of cypermethrin was elucidated by molecular docking. In addition, comet assay technique was applied to detect and quantify DNA damage at the cell level. For this aim, body and organ weights, aspartate aminotransferase (AST), alanine aminotransferase (ALT), malondialdehyde (MDA), glutathione (GSH), blood urea nitrogen (BUN) and creatinine levels, mitotic index (MI), DNA fragmentation, frequency of micronucleus (MN) and chromosomal aberrations (CAs) were used as indicators of toxicity. Mice were divided into 4 groups. The control group was fed with tap water and the administration groups were orally exposed to 62.5, 125 and 250 mg/kg b.w cypermethrin for 28 days. Then, the mice were sacrificed and tissue samples were collected. Cypermethrin caused a decrease in body and organ weights, GSH levels and MI and an increase in AST, ALT, MDA, BUN, creatinine levels and the frequency of MN and CAs (break, ring, gap, acentric, etc.). Cypermethrin promoted MN formation in leukocyte, erythrocyte, buccal mucosa epithelial cells. CAs and MN formation promoted by cypermethrin have been associated with DNA-cypermethrin interactions. This interaction has been demonstrated by simulation with molecular docking method and experimentally by spectral measurements of DNA. As a result, all three doses of cypermethrin caused toxicity in different cell types. In other words, the effect of cypermethrin taken into the body was not limited to only one cell type or region. Therefore, cypermethrin is a pyrethroid insecticide that promotes multifaceted toxicity in non-target organisms.