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Oxidative Medicine and Cellular Longevity
Volume 2016 (2016), Article ID 9895245, 17 pages
Research Article

Functionalized Fullerene Increases NF-κB Activity and Blocks Genotoxic Effect of Oxidative Stress in Serum-Starving Human Embryo Lung Diploid Fibroblasts

1Research Centre for Medical Genetics (RCMG), Moscow 115478, Russia
2V. A. Negovsky Research Institute of General Reanimatology, Moscow 107031, Russia
3Institute for Problems of Chemical Physics of Russian Academy of Sciences, Moscow Region 142432, Russia
4Skolkovo Institute of Science and Technology, Skolkovo Innovation Center, Nobel Street 3, Moscow 143026, Russia
5N. I. Pirogov Russian National Research Medical University, Moscow 117997, Russia

Received 25 December 2015; Revised 19 May 2016; Accepted 25 May 2016

Academic Editor: Javier Egea

Copyright © 2016 E. S. Ershova et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The influence of a water-soluble [] fullerene derivative containing five residues of 3-phenylpropionic acid and a chlorine addend appended to the carbon cage (F-828) on serum-starving human embryo lung diploid fibroblasts (HELFs) was studied. Serum deprivation evokes oxidative stress in HELFs. Cultivation of serum-starving HELFs in the presence of 0.1–1 µM F-828 significantly decreases the level of free radicals, inhibits autophagy, and represses expression of NOX4 and NRF2 proteins. The activity of NF-κB substantially grows up in contrast to the suppressed NRF2 activity. In the presence of 0.2–0.25 µM F-828, the DSB rate and apoptosis level dramatically decrease. The maximum increase of proliferative activity of the HELFs and maximum activity of NF-κB are observed at these concentration values. Conclusion. Under the conditions of oxidative stress evoked by serum deprivation the water-soluble fullerene derivative F-828 used in concentrations of 0.1 to 1 µM strongly stimulates the NF-κB activity and represses the NRF2 activity in HELFs.