Cytotoxic responses to 405Â nm light exposure in mammalian and bacterial cells: Involvement of reactive oxygen species

- Exposure to increasing doses of 405 nm light increases cell reactive oxygen species production in cells.
- 405 nm light exposures at higher doses induce cytotoxicity.
- Free radical scavengers offer cytoprotection at toxic exposure levels of 405 nm light.
- 405 nm light induced cytotoxicity is attributed to reactive oxygen species - mainly H2O2 - production and oxidative stress.

Light at wavelength 405 nm is an effective bactericide. Previous studies showed that exposing mammalian cells to 405 nm light at 36 J/cm2 (a bactericidal dose) had no significant effect on normal cell function, although at higher doses (54 J/cm2), mammalian cell death became evident. This research demonstrates that mammalian and bacterial cell toxicity induced by 405 nm light exposure is accompanied by reactive oxygen species production, as detected by generation of fluorescence from 6-carboxy-2′,7′-dichlorodihydrofluorescein diacetate. As indicators of the resulting oxidative stress in mammalian cells, a decrease in intracellular reduced glutathione content and a corresponding increase in the efflux of oxidised glutathione were observed from 405 nm light treated cells. The mammalian cells were significantly protected from dying at 54 J/cm2 in the presence of catalase, which detoxifies H2O2. Bacterial cells were significantly protected by sodium pyruvate (H2O2 scavenger) and by a combination of free radical scavengers (sodium pyruvate, dimethyl thiourea (OH scavenger) and catalase) at 162 and 324 J/cm2. Results therefore suggested that the cytotoxic mechanism of 405 nm light in mammalian cells and bacteria could be oxidative stress involving predominantly H2O2 generation, with other ROS contributing to the damage.