Abstract. The spatial dynamics of the optical emission from an array of 50 times 50 individual micro cavity plasma devices are investigated. The array is operated in argon and argon-neon mixtures close to atmospheric pressure with an AC voltage. The optical emission is analysed with phase and space resolution. It has been found that the emission is not continuous over the entire AC period, but occurs once per half period. Each of the observed emission phases shows a self-pulsing of the discharge, with several bursts of emission of fixed width and repetition rate. The number of emission bursts depends on applied voltage and frequency. Spatially resolved measurements prove that the emission bursts are formed by overlapping emission pulses from single discharge cavities. Intensity differences between positive and negative half-wave can be interpreted through spatially resolved measurements of single discharge cavities.

In previous studies, polyamine depletion by DFMO (alpha-difluoromethylornithine)-treatment reduced H(2)O(2)-induced apoptotic cell death by reduction of ferric ion uptake. In the present study, we analyzed the reduction of radiation-induced cell death by polyamine depletion. Exposure of HT29 cells to radiation induced severe cell death, but when cells were pretreated with DFMO, a specific inhibitor of polyamine biosynthesis, radiation-induced cell death was reduced to 50-60% of control. Cell cycle analysis showed that, in these cells, the time to reach the G(2)/M phase arrest was delayed for 20-24 h compared to the control cells, at which stage the fate of cells exposed to ionizing radiation is determined. DFMO-treated cells also showed a low level of thioredoxin, which is a high-level determinant of the cellular fate. To investigate the relationship between the G(2)/M phase arrest and the reduction of thioredoxin caused by polyamine depletion, we also analyzed thioredoxin-antisensed (asTRX) HT29 cells as for DFMO-treated cells. In asTRX-transfected cells, the gamma-irradiation-induced G(2)/M phase arrest was also significantly delayed and radiation-induced cell death was profoundly reduced, as in the DFMO-treated cells. Both sets of cells showed a decrease of cyclin D1 and an increment of HSP25, which are involved in radiation-induced cell cycle progress. Overall, these results suggest that polyamines are essential for normal cell death of HT29 cells triggered by gamma-radiation and that this is partially mediated by the regulation of thioredoxin expression.