Unraveling the acute sublethal effects of acetamiprid on honey bee neurological redox equilibrium

Abstract

Understanding the off-target effects of neonicotinoid insecticides, including acetamiprid, which is the most commonly applied agricultural chemical, is crucial as it may be an important factor of negative impact on pollinator insects causing a number of problems such as colony collapse disorder (CCD) of honey bees. While CCD is known as a multifactorial disease, the role of pesticides in this context is not negligible. Therefore, it is essential to gain a deeper comprehension of the mechanisms through which they function. The aim of this research was to study the effects of sublethal acetamiprid doses on honey bees, specifically focusing on the redox homeostasis of the brain. According to our findings, it can be confirmed that acetamiprid detrimentally impacts the redox balance of the brain increasing hydrogen peroxide and malondialdehyde levels, suggesting consequential lipid peroxidation and membrane damage as consequences. Moreover, acetamiprid had negative effects on the glutathione system and total antioxidant capacity, as well as key enzymes involved in the maintenance of redox homeostasis. In summary, it can be concluded that acetamiprid adversely affected the redox balance of the central nervous system of honey bees in our study. Our findings could potentially contribute to a better understanding of pesticide-related consequences and to improvement of bee health.

Keywords: Apis mellifera; Colony collapse disorder; Glutathione; Malondialdehyde; Neonicotinoids; Oxidative stress.

Fig. 1

Redox parameters measured in honey bee brain samples. Concentrations of (A) xanthine oxidase, (B) hydrogen peroxide, (C) malondialdehyde, (D) protein carbonyl, (E) 8-hydroxydeoxyguanosine, respectively. Data are visualized using violin plots, where dotted lines indicate median and solid lines indicate the first (Q1) and third (Q3) quartiles. “Control” refers to control group with no treatment; “AcetLow”, “AcetMedium” and “AcetHigh” refer to 2.076, 4.156 and 8.305 μg/bee/day acetamiprid exposure, respectively. Significant differences between control and acetamiprid exposed groups are indicated with asterisks. *P < 0.05, **P < 0.01, ***P < 0.001.

Fig. 2

Redox parameters measured in honey bee brain samples. Activities of (A) glucose-6-phosphate dehydrogenase, (B) superoxide dismutase, (C) total antioxidant capacity, respectively. Data are visualized using violin plots, where dotted lines indicate median and solid lines indicate the first (Q1) and third (Q3) quartiles. “Control” refers to control group with no treatment; “AcetLow”, “AcetMedium” and “AcetHigh” refer to 2.076, 4.156 and 8.305 μg/bee/day acetamiprid exposure, respectively. Significant differences between control and acetamiprid exposed groups are indicated with asterisks. **P < 0.01, ***P < 0.001.

Fig. 3

Redox parameters measured in honey bee brain samples. Concentrations of (A) reduced glutathione, (B) oxidized glutathione, (C) GSH-GSSG ratio, (D) total glutathione, respectively. Data are visualized using violin plots, where dotted lines indicate median and solid lines indicate the first (Q1) and third (Q3) quartiles. “Control” refers to control group with no treatment; “AcetLow”, “AcetMedium” and “AcetHigh” refer to 2.076, 4.156 and 8.305 μg/bee/day acetamiprid exposure, respectively. Significant differences between control and acetamiprid exposed groups are indicated with asterisks. *P < 0.05, **P < 0.01, ***P < 0.001.