A PVP-stabilized cerium oxide-platinum nanocomposite synthesized in TEG: pro-/antioxidant activities

Abstract

Cerium oxide nanoparticles (CeNPs) represent a highly promising material for a number of chemical and biological applications involving oxidation-reduction processes. However, the impact of synthesis conditions, as well as the incorporation of synergistic agents of a different catalytic nature, on the antioxidant or prooxidant properties of CeNPs remains a subject of ongoing investigation. In this study, non-stoichiometric CeNPs (∼10% Ce³⁺) stabilized by polyvinylpyrrolidone (PVP) were synthesized through the thermal autoxidative decomposition of cerium(iii) nitrate in a high-boiling glycol. A novel approach for the synthesis of CeNPs in the absence of additives (PVP-CeNPs) and with platinum (PVP-CeNPs-Pt), followed by the formation of platinum nanoparticles (PVP-PtNPs), was employed in a stepwise one-pot process. In chemical tests, the PVP-CeNPs-Pt nanocomposite exhibited enhanced peroxidase-mimicking activity and accelerated the Fenton-type reaction of dye decolorization. Nevertheless, it was found to have the ability to reduce adrenaline autoxidation via the superoxide dismutase-mimicking pathway. In vitro studies demonstrated that PVP-CeNPs and PVP-CeNPs-Pt enhanced H₂O₂-induced oxytosis while restoring cellular metabolic activity inhibited by the Fenton-like pathway of cellular apoptosis (ferroptosis) initiated by sulfasalazine. The authors suggest that the oxidoreductase activity of CeNP-based systems in the chemical tests and in biological processes in vitro may be caused by different mechanisms, which are discussed.

Fig. 1. (a) Schematic view of PVP-CeNPs–Pt nanocomposite synthesis by the high-temperature TEG process. (b) Dynamics of cerium species changes in the absorption spectrum of cerium(iii) nitrate TEG solution in the absence of PVP during heating. (c) UV-vis absorption spectra of PVP-CeNPs, PVP-CeNPs–Pt (2 wt% Pt), and PVP-PtNPs. The concentration of NPs was the same for all samples.

Fig. 2. (Top) TEM micrograph of (a) PVP-CeNPs, (b) PVP-PtNPs, and (c) PVP-CeNPs–Pt nanocomposites. (Bottom) The Pt 4f, Ce 3d, and O 1s core level photoelectron spectra for all samples.

Fig. 3. (a1–a4) Kinetics of MB decomposition by Fenton's reaction at pH 7.0. (b1–b4) Kinetics of IC decomposition by hydrogen peroxide at pH 7.0. (c1–c4) Dynamics of MB bleaching by hypochlorite at pH 7.0. (d1–d4) Dynamics of adrenaline autooxidation at pH 10.5. (a1, b1, c1 and d1) PVP-CeNPs, (a2, b2, c2 and d2) PVP-CeNPs–Pt, (a3, b3, c3 and d3) PVP-PtNPs, (a4, b4, c4 and d4) summarized data. The concentration of NPs in mM units for each experiment is given in the legend or on the abscissa of the corresponding figure. The concentration of PVP-PtNPs is the same as for PVP-CeNPs–Pt nanocomposites, but without CeNPs.

Fig. 4. Metabolic activity (MTT), viability (CV), and the index of metabolic activity (IMA) of MA-104 cells in the presence of PVP-CeNPs, PVP-CeNPs–Pt, and PVP-PtNP sols prepared by double dilution with water.

Fig. 5. (a, orange) Viability in TB exclusion assay, (b, orange) metabolic activity in MTT assay, (a, b, blue) viability of adherent cells in CV assay, and (a, black) index of viability (TB/CV) and (b, black) index of metabolic activity (IMA) of MA-104 cells in the presence of different concentrations of PVP-CeNPs, PVP-CeNPs–Pt, and PVP-PtNP sols under the condition of: (a) oxytosis caused by H₂O₂ during (a1, a2 and a3) prophylactic and (a4, a5 and a6) therapeutic regimens; (b) ferroptosis caused by sulfasalazine (SAS) during (b1, b2 and b3) preventive and (b4, b5, b6) therapeutic regimens. The concentration of CeNPs in PVP-CeNPs–Pt is identical to that in PVP-CeNPs.