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3,4-Dimethoxyphenyl bis-benzimidazole derivative, mitigates radiation-induced DNA damage.

Authors
  • Ranjan, Atul
  • Kaur, Navrinder
  • Tiwari, Vinod
  • Singh, Yogendra
  • Chaturvedi, Madan Mohan
  • Tandon, Vibha
Type
Published Article
Journal
Radiation Research
Publisher
BioOne (Radiation Research Society)
Publication Date
Jun 01, 2013
Volume
179
Issue
6
Pages
647–662
Identifiers
DOI: 10.1667/RR3246.1
PMID: 23642081
Source
Medline
License
Unknown

Abstract

Radiation-induced DNA damage initiates a series of overlapping responses that include DNA damage recognition and repair, induction of cell cycle checkpoints, senescence and/or apoptosis. This study assessed the DNA damage response and whole genome expression profile in two mammalian cell lines (HEK and U87) in response to (5-{4-methylpiperazin-1-yl}-2-[2'-(3,4-dimethoxyphenyl)-5'-benzimidazolyl] benzimidazole) DMA and ionizing radiation. DMA has been shown to act as a potent radiation protector, yielding significant levels of protection, i.e., 20.9% in HEK cells and 21.2% in U87 cells. Our findings revealed treatment with DMA significantly reduced γ-H2AX, 53BP1 and Rad51 foci formation after irradiation. MAP kinase, WNT signaling and p53 pathways were found to be activated in DMA-treated cells. In addition, the DNA damage response genes, HSP70, HSPD1, PRDX1, PRX, CALR, NPM, UBC, and SET showed differential regulation in DMA, DMA + radiation and radiation-treated cells. The data suggest that DMA-influenced repertoire of repair proteins, which are an indispensable part of the cell, interplay with each other to reduce DNA damage and maintain the genomic integrity of the cell.

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