Data for In vitro effects of Taurine on Taxol-induced mitochondrial dysfunction

Mitochondria are intricately involved with many essential functions in normal and cancer cells and, as such, mitochondria are a natural target for chemotherapeutic drugs. We previously showed that Taxol, even at low doses, adversely effects mitochondrial energetics, function, and intracellular migration patterns. We observed (by multiple optical means) suppression of oxidative phosphorylation (OXPHOS) and decrease of adenosine triphosphate (ATP) production, increase of mitochondrial reactive oxygen species (ROS) generation (both immediately and integrated over time), increased mitotic fraction, and release of LDH and cytochrome c in Taxol-treated cells. Moreover, we observed more random (less ordered) motion of the mitochondria as well as altered mitochondrial morphology and lessened association with microtubules. Recently, several in vitro and in vivo studies have demonstrated the beneficial effects of taurine (a ubiquitously expressed non-protein amino acid in most tissues, particularly in the heart, retina, brain and muscles) in maintaining mitochondrial functions. Intracellular concentrations of taurine ranges from 5–50 mM, but most cell culture media do not include taurine. In this study, we show how taurine supplementation affects the impact of low level Taxol treatment in a variety of cell lines with varying glycolytic profiles. A549 (non-small cell lung epithelial cancer cell line), A549-ñ0 (mitochondrial DNA-depleted derivative of A549), BEAS-2B (a non-cancer cell line derived from normal bronchial epithelium), as well as T98G (glioblastoma cell line) cells are used in this study.