Posted on the website on 9 November 2004.
Endogenous Fluorescence Spectroscopy of Cell Suspensions for Chemopreventive Drug Monitoring¶
Article first published online: 23 MAY 2007
Photochemistry and Photobiology
Volume 81, Issue 1, pages 125–134, January 2005
How to Cite
Kirkpatrick, N. D., Zou, C., Brewer, M. A., Brands, W. R., Drezek, R. A. and Utzinger, U. (2005), Endogenous Fluorescence Spectroscopy of Cell Suspensions for Chemopreventive Drug Monitoring. Photochemistry and Photobiology, 81: 125–134. doi: 10.1111/j.1751-1097.2005.tb01531.x
- Issue published online: 23 MAY 2007
- Article first published online: 23 MAY 2007
- Received 6 August 2004; accepted 27 October 2004
Cancer chemopreventive agents such as N-4-(hydroxyphenyl)-retinamide (4HPR) are thought to prevent cancers by suppressing growth or inducing apoptosis in precancerous cells. Mechanisms by which these drugs affect cells are often not known, and the means to monitor their effects is not available. In this study endogenous fluorescence spectroscopy was used to measure metabolic changes in response to treatment with 4HPR in ovarian and bladder cancer cell lines. Fluorescence signals consistent with nicotinamide adenine dinucleotide (NADH), flavin adenine dinucleotide (FAD) and tryptophan were measured to monitor cellular activity through redox status and protein content. Cells were treated with varying concentrations of 4HPR and measured in a stable environment with a sensitive fluorescence spectrometer. Results suggest that redox signal of all cells changed in a similar dose-dependant manner but started at different baseline levels. Redox signal changes depended primarily on changes consistent with NADH fluorescence, whereas the FAD fluorescence remained relatively constant. Similarly, tryptophan fluorescence decreased with increased drug treatment, suggesting a decrease in protein production. Given that each cell line has been shown to have a different apoptotic response to 4HPR, fluorescence redox values along with changes in tryptophan fluorescence may be a response as well as an endpoint marker for chemopreventive drugs.