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Published on: July 8, 2015
Carbon@CeO2 nanocomposites modulate ROS homeostasis in UV-exposed bone marrow cells
Veronika Sarnatskaya1, Petro Virych1, Yuliia Shlapa2
1R.E. Kavetsky Institute of Experimental Pathology, Oncology and Radiobiology of the NAS 45, Vasylkivska St. Kyiv 03022 Ukraine vsnikavera@gmail.com.
None:
The development of advanced nanomaterials capable of modulating cellular redox homeostasis is critical for photoprotection and regenerative medicine. This study presents a comprehensive evaluation of a hybrid "carbon-cerium dioxide nanocomposite" (C@CeO2) designed to mitigate 390 nm UV-induced oxidative stress in mouse bone marrow cells (MBMCs). Using a multi-parametric approach, we demonstrate that while pristine carbon particles (CPs) exacerbate photo-oxidative damage at high concentrations, the integration of catalytic CeO2 nanoparticles (NPs) into a carbon matrix creates a synergistic "shielding" effect. Morphometric analysis revealed that the C@CeO2 composite significantly attenuates UV-induced cellular hypertrophy and morphological distortion, maintaining baseline cell area and circularity. Mechanistically, flow cytometric analysis using JC-1 and Annexin V/7-AAD uncovered a sophisticated phenotypic dissociation: the hybrid system decouples mitochondrial depolarization from terminal apoptotic commitment. This cytoprotection is further supported by metabolic profiling, which identified a Warburg-like shift toward aerobic glycolysis; C@CeO2 effectively normalized glucose homeostasis and maintained high glycolytic flux (lactate efflux) despite mitochondrial stress, providing a metabolic "backup generator" for cellular survival. Immunocytochemical profiling of the p53/p21, Bcl-2, and Wnt/β-catenin axes confirms that the nanocomposite reprograms the intracellular regulatory network, upregulating anti-apoptotic signaling (Bcl-2) and maintaining genomic surveillance. These findings demonstrate that C@CeO2 does not merely scavenge reactive oxygen species but actively modulates cellular adaptation to acute stress. This hybrid architectural approach offers a superior cytoprotective strategy, enabling highly effective radioprotection against UV-induced damage at low nanocomposite doses through synergistic shielding and catalytic redox activity rather than high material concentrations, with significant implications for biomedicine and the development of redox-active biomaterials.
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