DIFFERENTIAL EFFECTS OF ZnO AND Ag NANOPARTICLES, AND DIAZINON ON THE ACTIVITY OF MEMBRANE AND SOLUBLE FORM OF ACETYLCHOLINESTERASE IN HONEY BEE HEAD AND THORAX
1 University of Ljubljana, Biotechnical Faculty, Department of Biology, Vecˇna pot 111, Ljubljana SI-1000, Slovenia
2 Centre of Excellence in Advanced Materials and Technologies for the Future (CO NAMASTE), Jozef Stefan Institute, Jamova 39, SI-1000 Ljubljana, Slovenia
3 Centre of Excellence in Nanoscience and Nanotechnology (CO Nanocenter), Jozef Stefan Institute, Jamova 39, SI-1000 Ljubljana, Slovenia
Honey bee is an important pollinator threatened by diverse environmental factors, potentially also by products of nanotechnologies. Deliberate application of nanopesticides will result in inputs of engineered nanoparticles into the environment, entering both soil and freshwater environments. The activity of soluble form of acetylcholinesterase (AChE) is often used as an important biomarker of neurotoxicity after exposure to xenobiotics. Recently, in vitro experiments suggested that the membrane form of AChE is mainly neuronal whereas the role of soluble form is largely unknown, but some suggestions of their protective role against xenobiotics have been given. Therefore, in regard to neurotoxicity, monitoring of only soluble AChE is not sufficient. In this study we investigated in vivo effects of ZnO NPs (500 mg/L, sucrose feeding) and Ag nanoparticles (NPs) (50 mgL, sucrose feeding) and AChE inhibitor diazinon (1.5 mg/L, sucrose feeding) not only on the activity of soluble AChE, but also membrane AChE in honey bee head and thorax. The activity of membrane AChE in the head of untreated honey bees was much higher that the soluble confirming results of in vitro experiments showing that the membrane form is probably neuronal. In the thorax this ratio was much lower. The chronic 10 days exposure to ZnO NPs and Ag NPs elevated the activity of the soluble, but not the membrane AChE in the head. However, the same treatment had no effect of any form of AChE in the thorax. On contrary, the chronic exposure to AChE inhibitor diazinon diminished only the activity of soluble AChE in the head, but unexpectedly elevated the soluble AChE in the thorax. Our results indirectly confirm the difference in the function of two forms of AChE. The elevation of the activity of soluble AChE might be predictable for its detoxifying function whereas the changes in the activity of membrane AChE could be the result of the compensatory effect of nervous system or direct inhibition by diazinon. However, the role of the soluble AChE needs to be further investigated. We show that the mechanism of ZnO NPs and Ag NPs action on AChE is similar but other than the mechanism of diazinon suggesting that ZnO and Ag NPs don’t act directly inhibitory on AChE at the exposure set-up (doses, and duration) used in our experiment.