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3 May 2013 3,4-Dimethoxyphenyl Bis-benzimidazole Derivative, Mitigates Radiation-Induced DNA Damage
Atul Ranjan, Navrinder Kaur, Vinod Tiwari, Yogendra Singh, Madan Mohan Chaturvedi, Vibha Tandon
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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.

Atul Ranjan, Navrinder Kaur, Vinod Tiwari, Yogendra Singh, Madan Mohan Chaturvedi, and Vibha Tandon "3,4-Dimethoxyphenyl Bis-benzimidazole Derivative, Mitigates Radiation-Induced DNA Damage," Radiation Research 179(6), 647-662, (3 May 2013). https://doi.org/10.1667/RR3246.1
Received: 5 November 2012; Accepted: 1 November 2012; Published: 3 May 2013
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