Abstract
In this manuscript, we have reported how DNA binding of ruthenium polypyridyl complexes (RPCs) make them more efficient photosensitizer. The DNA binding of RPCs results in a significant enhancement of their emission intensity and excited-state lifetime. As a result, upon visible-light irradiation, these complexes generate reactive singlet oxygen, which causes selective DNA damage and kills cancer cells. This investigation also demonstrates the effect of light-driven RPCs on bacterial growth arrest through DNA nicking and differential localization in cancer and non-cancer cells. The local DNA microviscosity suppresses the non-radiative pathways which causes a large enhancement in the emission intensity and the excited state lifetime. The visible-light-triggered singlet-oxygen efficiently produces nick in DNA and inhibits bacterial growth. RPCs also localize inside the cancer cell nucleus and in the vicinity of the nuclear membrane of non-cancerous cells, confirmed by live-cell confocal microscopy. The results provide a facile platform for the novel antibiotic intended discovery combined with cancer therapy.
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