Carbonaceous materials derived from corn cob waste via pyrolysis, hydrothermal carbonization and open burning:...

Here, three different types of carbonaceous nanoparticles/materials were obtained from corn cob agricultural waste using different "green" approaches without surface functionalization. Biochars synthesized from corn cobs by two-step pyrolysis at 600 °C (PB), carbon dots synthesized using a hydrothermal approach at 180 °C (CD) and smoke particulate matter (SP) prepared by open burning were comparatively analyzed for biocompatibility and Cu²⁺ adsorption capacity using a presynaptic rat cortex nerve terminal model (synaptosomes). The PB did not change the extrasynaptosomal levels of inhibitory neurotransmitter [³H]GABA and excitatory neurotransmitter L-[³H]glutamate within the concentration range of 0.1-1.0 mg mL^-1, while the CD and SP increased the extrasynaptosomal levels of these neurotransmitters starting from the concentrations of 0.5 and 0.1 mg mL^-1, respectively. In a fluorimetric study, the PB did not change the mitochondrial membrane potential of nerve terminals, while both the CD and SP significantly depolarized the mitochondrial membrane. Using an animal model of acute heavy metal-induced neurotoxicity, different capability of carbonaceous materials to influence Cu²⁺-induced neurotoxicity was found. In particular, the PB significantly mitigated Cu²⁺-induced damaging effects on the extrasynaptosomal neurotransmitter levels, while the CD and SP further increased Cu²⁺-induced neurotoxicity in a synergistic manner. In fluorimetric measurements of the plasma membrane and mitochondrial membrane potential, the PB mitigated Cu²⁺-induced membrane depolarization, while the CD and SP further depolarized the membranes of nerve terminals in a synergistic manner. Moreover, the PB and CD/SP showed different effects on ROS generation in nerve terminals. Therefore, three carbonaceous nanoparticles/materials obtained from corn cob waste using different "green" methods demonstrated different biocompatibility profiles and opposite modulatory effects on Cu²⁺-induced neurotoxicity in the nerve terminal model.