Graphene Quantum Dots Protect against Copper Redox-Mediated Free Radical Generation and Cardiac Cell Injury

  • Y. Robert Li Department of Pharmacology, Campbell University Medical School, Buies Creek, NC 27506, USA; Department of Pharmaceutical Sciences, Campbell University College of Pharmacy and Health Sciences, Buies Creek, NC 27506, USA; Department of Biology, University of North Carolina College of Arts and Sciences, Greensboro, NC 27412, USA; Virginia Tech‒Wake Forest University School of Biomedical Engineering and Sciences, Blacksburg, VA 24061, USA; Department of Biomedical Sciences and Pathobiology, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061, USA
  • Arben Santo Department of Pathology, EVCOM, Virginia Tech CRC, Blacksburg, VA 24060, USA
  • Hong Zhu Department of Physiology and Pathophysiology, Campbell University Medical School, Buies Creek, NC 27506, USA
  • Zhenquan Jia Department of Pharmacology, Campbell University Medical School, Buies Creek, NC 27506, USA; Department of Pharmaceutical Sciences, Campbell University College of Pharmacy and Health Sciences, Buies Creek, NC 27506, USA; Department of Biology, University of North Carolina College of Arts and Sciences, Greensboro, NC 27412, USA
  • Michael A. Trush Department of Environmental Health and Engineering, The Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD 21205, USA
Keywords: Copper redox; Electron paramagnetic resonance; Graphene quantum dots; Human cardiomyocytes; Hydrogen peroxide; Hydroxyl radical; Hydroquinone; Nanotechnology; Oxygen polarography; Spin-trapping

Abstract

In this work, we investigated the effects of graphene quantum dots (GQDs) on copper redox-mediated free radical generation and cell injury. Using electron paramagnetic resonance (EPR) spectrometry in conjunction with 5,5-dimethyl-1-pyrroline N-oxide (DMPO) as a spin trap, we found that GQDs at a concentration as low as 1 µg/ml significantly inhibited Cu(II)/H2O2-mediated hydroxyl radical formation. GQDs also blocked Cu(II)-catalyzed nucleophilic addition of H2O to DMPO to form a DMPO-OH adduct in the absence of H2O2, suggesting a potential for GQDs to inhibit copper redox activity. Indeed, we observed that the presence of GQDs prevented H2O2-mediated reduction of Cu(II) to Cu(I) though GQDs themselves also caused the reduction of Cu(II) to Cu(I). To further investigate the effects of GQDs on copper redox activity, we employed the Cu(II)/hydroquinone system in which copper redox activity plays an essential role in the oxidation of hydroquinone to semiquinone radicals with consequent oxygen consumption. Using oxygen polarography as well as EPR spectrometry, we demonstrated that the presence of GQDs drastically blocked the oxygen consumption and semiquinone radical formation resulting from the reaction of Cu(II) and hydroquinone. These results suggested that GQDs suppressed free radical formation via inhibiting copper redox activity. Lastly, using cultured human cardiomyocytes, we demonstrated that the presence of GQDs also protected against Cu(II)/H2O2-mediated cardiac cell injury as indicated by morphological changes (e.g., cell shrinkage and degeneration). In conclusion, our work shows, for the first time, the potential for using GQDs to counteract copper redox-mediated biological damage.

Published
2018-09-01
How to Cite
Li, Y. R., Santo, A., Zhu, H., Jia, Z., & Trush, M. A. (2018). Graphene Quantum Dots Protect against Copper Redox-Mediated Free Radical Generation and Cardiac Cell Injury. Reactive Oxygen Species, 6(17), 338–348. Retrieved from https://aimsci.com/ros/index.php/ros/article/view/158
Section
Original Research Articles