Induction of A549 Nonsmall‐Cell Lung Cancer Cells Proliferation by Photoreleased Nicotine

Caged compounds comprise the group of artificially synthesized, light‐sensitive molecules that enable in situ derivation of biologically active constituents capable of affecting cells, tissues and/or biological processes upon exposure to light. Ruthenium‐bispyridine (RuBi) complexes are photolyzed by biologically harmless visible light. In the present study, we show that RuBi‐caged nicotine can be used as a source of free nicotine to induce proliferation of A549 nonsmall‐cell lung cancer (NSCLC) cells by acting on nicotinic acetylcholine receptors expressed in these cells. RuBi‐nicotine was photolyzed using LED light source with the spectrum matching RuBi‐absorption. Photorelease of free nicotine ([Nic]p/r) was quantified by high‐performance liquid chromatography (HPLC). 5‐s‐long light exposure of 10 μm of RuBi‐nicotine generated 2 μm [Nic]p/r which enhanced A549 cell proliferation similarly to the 2 μm of plain nicotine during 72 h of cell culturing. Both RuBi‐nicotine per se and its photolysis byproduct exerted no effect on A549 cells. We conclude that RuBi‐nicotine can be a good source of free nicotine for inducing short‐ and long‐term biological effects. Photolysis of RuBi‐nicotine is quite effective, and can produce biologically relevant concentrations of nicotine at acceptable concentrations of the source material with the use of simple, inexpensive, and easily accessible light sources. Nicotine released as a result of RuBi‐nicotine photolysis promotes proliferation of A549 lung cancer cells via activation of nicotinic acetylcholine receptors (nAChR) expressed in cell plasma membrane.