Mercury-induced excitotoxicity in presynaptic brain nerve terminals: modulatory effects of carbonaceous airborne particulate simulants.

Multipollutant approach is a breakthrough in up-to-date environmental quality and health risk estimation. Both mercury and carbonaceous air particulate are hazardous neurotoxicants. Here, the ability of carbonaceous air particulate simulants, i.e. carbon dots obtained by heating of organics, and nanodiamonds, to influence Hg-induced neurotoxicity was monitored using biological system, i.e. presynaptic rat cortex nerve terminals. Using HgCl and classical reducing/chelating agents, an adequate synaptic parameter, i.e. the extracellular level of key excitatory neurotransmitter L-[C]glutamate, was selected for further analysis. HgCl starting from 5 µM caused an acute and concentration-dependent increase in the extracellular L-[C]glutamate level in nerve terminals. Combined application of Hg and carbon dots from heating of citric acid/urea showed that this simulant was able to mitigate in an acute manner excitotoxic Hg-induced increase in the extracellular L-[C]glutamate level in nerve terminals by 37%. These carbon dots and Hg acted as a complex in nerve terminals that was confirmed with fluorimetric data on Hg-induced changes in their spectroscopic features. Nanodiamonds and carbon dots from β-alanine were not able to mitigate a Hg-induced increase in the extracellular L-[C]glutamate level in nerve terminals. Developed approach can be applicable for monitoring capability of different particles/compounds to have Hg-chelating signs in the biological systems. Therefore, among testing simulants, the only carbon dots from citric acid/urea were able to mitigate acute Hg-induced neurotoxicity in nerve terminals, thereby showing a variety of effects of carbonaceous airborne particulate in situ and its potential to interfere and modulate Hg-associated health hazard.