Molecular Mechanism of Action of Abamectin on Human Microglia Clone 3 Cell Line

Abstract

Introduction:

Abamectin (ABA) is an insecticide that is commonly used in agricultural spraying. Although it is known to have neurotoxic effects on living organisms in the ecosystem and humans, the details of these effects, including the duration and amount of exposure, are not fully understood. The aim of this study is to evaluate the effect of ABA exposure on human microglia clone 3 (HMC3) cells. These cells were chosen because they are suitable for modeling immunological functions such as cytokine production, cell migration, and inflammation response.

Materials and Methods:

The impact of ABA on the viability of HMC3 cells was evaluated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, while the effect of ABA on Interleukin-18 (IL-18) levels was assessed through enzyme-linked immunosorbent assay. Furthermore, the influence of ABA on apoptosis parameters was determined through qRT-PCR.

Results:

Increasing concentrations of ABA were observed to decrease the viability of HMC3 cells. The IC₅₀ dose was determined to be 25.71 μg/mL. IC₅₀: 25.71 μg/mL and half of IC₅₀ doses (IC_50/2: 12.85 μg/mL) were applied to the cells. The results of the dose applications were compared with the results of the control groups. There was a significant increase in IL-18 levels in cells treated with 25.71 μg/mL ABA (p < 0.001). There was a significant increase in p53 and BAD expression levels in cells treated with 25.71 μg/mL ABA (p < 0.05). There was a significant decrease in BCL2L1 expression levels in cell treated with 25.71 and 12.85 μg/mL ABA (p < 0.05).

Conclusions:

These results clearly demonstrate that it can be concluded that ABA exposure caused a decrease in the survival of HMC3 cells and induced apoptosis. Long-term exposure to ABA may increase the risk of neurodegenerative diseases as a result of inflammation and decreased cell viability.