Veterinary session

There has been a drastic decline in the honeybee populations over the last decades, which is a serious problem in ecological aspects as well as for agricultural economy. One of the reasons for the disappearance of this species is the so-called Colony Collapse Disorder (CCD). Several factors’ combined impacts cause this disease, from which the exposure to different pesticides as the result of intensive agriculture are of particular importance. Acetamiprid is a neonicotinoid insecticide, which thought to be environmentally safe, therefore extensively used worldwide. Further research of the effects on honeybees is essential, as negative consequences have been reported in numerous studies, but none explained the underlying cellular processes.

This study is focusing on the acute, sublethal effects of acetamiprid on redox homeostasis of western honeybees’ (Apis mellifera) central nervous system. 50-50 individuals of each treatment group were involved in our experiment, that received different concentrations of acetamiprid ad libitum via the feeding solution (8.75 mg/l; 17.5 mg/l and 35 mg/l). In the samples we got after 48 hours of treatment, the presence and the extent of the occurring oxidative stress was monitored, measuring several biological markers and antioxidant enzyme activities. Therefore, the measurement of the following parameters has been carried out: concentrations of hydrogen peroxide (H2O2), malondialdehyde (MDA), glutathione (GSH-GSSG); activities of glucose-6-phosphate dehydrogenase (G6PDH) and superoxide dismutase (SOD) enzymes.

Our results showed a significant increase in the concentrations of H2O2 in all treatment groups. MDA, which is a parameter that indicates lipid peroxidation and membrane damage, also showed a significant increase in all groups. The GSH-GSSG ratio decreased significantly, which indicates the depletion of the glutathione system responsible for maintaining redox homeostasis. G6PDH is a regulatory enzyme of the pentose phosphate pathway, whose activity decreased significantly after the treatment. We found a significant decrease in the activity of SOD as the effect of the highest treatment concentration. SOD is a key enzyme for protection against oxidative stress, therefore this result may also indicate a disturbance of the antioxidant system.

The results of our research confirmed the hypothesis, that the exposure to acetamiprid causes oxidative stress in the honeybees’ central nervous system. This may also be involved in the cognitive impairment observed by other research groups. Our detailed study of acetamiprid may contribute to further understanding of the neonicotinoid-related harmful effects in pollinators, which may play a significant role in the development of CCD.