Defects are widely present in nanomaterials, and they are recognized as the active sites that tune surface properties in the local region for catalysis. Recently, the theory linking defect structures and catalytic properties of nanocatalysts has been most commonly described. In this study, we prepared boron-doped carbon nano-onions (B-CNOs) by applying an annealing treatment of ultradispersed nanodiamond particles and amorphous boron. These experimental conditions guarantee doping of CNOs with boron atoms in the entire carbon nanostructure, thereby ensuring structural homogeneity. In our research, we discuss the correlations between defective structures of B-CNOs with their catalytic properties toward SO₂ and tert-butanol dehydration. We show that there is a close relationship between the catalytic properties of the B-CNOs and the experimental conditions for their formation. It is not only the mass of the substrates used for the formation of B-CNOs that is crucial, that is, the mass ratio of NDs to amorphous B, but also the process, including temperature and gas atmosphere. As it was expected, all B-CNOs demonstrated significant catalytic activity in HSO₃^– oxidation. However, the subsequent annealing in an air atmosphere diminished their catalytic activity. Unfortunately, no direct relationship between the catalytic activity and the presence of heteroatoms on the B-CNO surface was observed. There was a linear dependence between catalytic activity and Raman reactivity factors for each of the B-CNO materials. In contrast to SO₂ oxidation, the B-CNO-a samples showed higher catalytic activity in tert-butanol dehydration due to the presence of Brønsted and Lewis acid sites. The occurence of three types of boron-Lewis sites differing in electron donor properties was confirmed using quantitative infrared spectroscopic measurements of pyridine adsorption.

Etiopathogenesis of migraine involves different structures of the central nervous system: the trigeminal nerve with nuclei located in the brain stem, vascular system, and the cerebral cortex as well as diverse mechanisms and pathological processes. The multidirectional action of purines in different cell types (blood vessels, neurons, and satellite glial cells) and through different types of purinergic receptors contributes to the etiopathogenesis of migraine pain. Adenosine triphosphate (ATP) and its derivatives are involved in initiation and propagation of migrenogenic signals in several ways: they participate in vasomotor mechanism, cortical spreading depression, and in fast transmission or cross-excitation based on the satellite glial cells in trigeminal ganglion. Contribution of purinergic signaling in the conduction of pain is realized through the activation of P1 and P2 receptors expressed widely in the central nervous system: on the neurons and glial cells as well as on the smooth muscles and endothelium in the vascular system. Therefore, the purinergic receptors can be an excellent target for pharmacologists constructing new antimigraine therapeutics. Moreover, the mechanisms facilitating ATP and adenosine degradation may prevent vasodilatation and thus avoid a secondary central sensitization during a migraine attack. Thus, agonists and antagonists of P receptors as well as ecto-enzymes metabolizing nucleotides/nucleosides could gain the growing attention as therapeutic agents.

The cytotoxic influence of two different carbonaceous nanomaterials on human mesenchymal stem cells (MSCs) cultured in vitro was compared in the short (1–3 days) and long term (up to 60 days). Amorphous carbon and single-walled carbon nanotubes were chosen and evaluated due to their contrasting physicochemical properties. Both materials, though supposed similarly low-toxic in basic short-term cytotoxicity assays, demonstrated dramatically different properties in the long-term study. The surface chemistry and biomolecule-adsorption capacity turned out to be crucial factors influencing cytotoxicity. We proved that amorphous carbon is able to weakly bind a low-affinity protein coat (so-called soft corona), while carbon nanotubes behaved oppositely. Obtained results from zeta-potential and adsorption measurements for both nanomaterials confirmed that a hard protein corona was present on the single-walled carbon-nanotube surface that aggravated their cytotoxic influence. The long-term exposure of the mesenchymal stem cells to carbon nanotubes, coated by the strongly bound proteins, showed a significant decrease in cell-growth rate, followed by cell senescence and death. These results are of great importance in the light of increasing nanomaterial applications in biomedicine and cell-based therapies. Our better understanding of the puzzling cytotoxicity of carbonaceous nanomaterials, reflecting their surface chemistry and interactions, is helpful in adjusting their properties when tailored for specific applications.

Carbon-based quantum dots are widely suggested as fluorescent carriers of drugs, genes or other bioactive molecules. In this work, we thoroughly examine the easy-to-obtain, biocompatible, nitrogen-containing carbonaceous quantum dots (N-CQDs) with stable fluorescent properties that are resistant to wide-range pH changes. Moreover, we explain the mechanism of fluorescence quenching at extreme pH conditions. Our in vitro results indicate that N-CQDs penetrate the cell membrane; however, fluorescence intensity measured inside the cells was lower than expected from carbonaceous dots extracellular concentration decrease. We studied the mechanism of quenching and identified reduced form of β-nicotinamide adenine dinucleotide (NADH) as one of the intracellular quenchers. We proved it experimentally that the elucidated redox process triggers the efficient reduction of amide functionalities to non-fluorescent amines on carbonaceous dots surface. We determined the 5 nm–wide reactive redox zone around the N-CQD surface. The better understanding of fluorescence quenching will help to accurately quantify and dose the internalized carbonaceous quantum dots for biomedical applications.