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Fullerene–polyvinylpyrrolidone clathrate localizes in the cytoplasm to prevent Ultraviolet‐A ray‐induced DNA‐fragmentation and activation of the transcriptional factor NF‐kappaB
Author(s) -
Xiao Li,
Aoshima Hisae,
Saitoh Yasukazu,
Miwa Nobuhiko
Publication year - 2010
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.22784
Subject(s) - hacat , cytoplasm , microbiology and biotechnology , chemistry , dna fragmentation , biology , apoptosis , biochemistry , programmed cell death , in vitro
By Western blot and immunostaining we proved that polyvinylpyrrolidone (PVP)‐wrapped fullerene molecules (PVP–fullerene) could combine the 8‐ and 53‐kb proteins which localize in the membrane of human skin keratinocytes HaCaT. Only fullerene molecules are able to cross the lipid membrane and conjugate 53‐kb proteins in the cytosol. There are no fullerene molecules detectable in the nucleus or cytoskeleton. Ultraviolet‐A (UVA)‐irradiation on HaCaT or normal human epidermal melanocytes (NHEM) caused nuclear fragmentations, lowering of intracellular DNA‐contents below diploidy, concurrently with the repressed DNA synthesis and the increased DNA‐3′OH cleavage terminals, all of which were repressed by PVP–fullerene, as shown by flow cytometry and PI‐ or TUNEL‐stain fluorography. Translocation of the transcriptional factor NF‐kappaB in the cytoplasm to the nucleus of the keratinocytes was caused with UVA and repressed by PVP–fullerene with cytoprotective effects. Thus, the PVP–fullerene may be developed as a UV‐protective agent with DNA‐preservative effects owing to its combinative ability to molecules in the cytoplasm and cytomembrane, and then represses cellular oxidative stress and blocks abnormal signal pathways. J. Cell. Biochem. 111: 955–966, 2010. © 2010 Wiley‐Liss, Inc.