CO diffusion and desorption kinetics in CO2_2 ices

Diffusion of species in icy dust grain mantles is a fundamental process that shapes the chemistry of interstellar regions; yet measurements of diffusion in interstellar ice analogs are scarce. Here we present measurements of CO diffusion into CO$_2$ ice at low temperatures (T=11--23~K) using CO$_2$ longitudinal optical (LO) phonon modes to monitor the level of mixing of initially layered ices. We model the diffusion kinetics using Fick's second law and find the temperature dependent diffusion coefficients are well fit by an Arrhenius equation giving a diffusion barrier of 300 $\pm$ 40 K. The low barrier along with the diffusion kinetics through isotopically labeled layers suggest that CO diffuses through CO$_2$ along pore surfaces rather than through bulk diffusion. In complementary experiments, we measure the desorption energy of CO from CO$_2$ ices deposited at 11-50 K by temperature-programmed desorption (TPD) and find that the desorption barrier ranges from 1240 $\pm$ 90 K to 1410 $\pm$ 70 K depending on the CO$_2$ deposition temperature and resultant ice porosity. The measured CO-CO$_2$ desorption barriers demonstrate that CO binds equally well to CO$_2$ and H$_2$O ices when both are compact. The CO-CO$_2$ diffusion-desorption barrier ratio ranges from 0.21-0.24 dependent on the binding environment during diffusion. The diffusion-desorption ratio is consistent with the above hypothesis that the observed diffusion is a surface process and adds to previous experimental evidence on diffusion in water ice that suggests surface diffusion is important to the mobility of molecules within interstellar ices

Nucleosomes indicate the in vitro radiosensitivity of irradiated bronchoepithelial and lung cancer cells

Nucleosomes, which are typical cell death products, are elevated in the serum of cancer patients and are known to rapidly increase during radiotherapy. As both normal and malignant cells are damaged by irradiation, we investigated to which extent both cell types contribute to the release of nucleosomes. We cultured monolayers of normal bronchoepithelial lung cells (BEAS-2B, n = 18) and epithelial lung cancer cells (EPLC, n = 18), exposed them to various radiation doses (0, 10 and 30 Gy) and observed them for 5 days. Culture medium was changed every 24 h. Subsequently, nucleosomes were determined in the supernatant by the Cell Death Detection-ELISA(plus) ( Roche Diagnostics). Additionally, the cell number was estimated after harvesting the cells in a second preparation. After 5 days, the cell number of BEAS-2B cultures in the irradiated groups (10 Gy: median 0.03 x 10(6) cells/culture, range 0.02-0.08 x 10(6) cells/culture; 30 Gy: median 0.08 x 10(6) cells/culture, range 0.02-0.14 x 10(6) cells/culture) decreased significantly (10 Gy: p = 0.005; 30 Gy p = 0.005; Wilcoxon test) compared to the non-irradiated control group (median 4.81 x 10(6) cells/culture, range 1.50-9.54 x 10(6) cells/culture). Consistently, nucleosomes remained low in the supernatant of nonirradiated BEAS-2B. However, at 10 Gy, BEAS-2B showed a considerably increasing release of nucleosomes, with a maximum at 72 h ( before irradiation: 0.24 x 10(3) arbitrary units, AU, range 0.13-4.09 x 10(3) AU, and after 72 h: 1.94 x 10(3) AU, range 0.11-5.70 x 10(3) AU). At 30 Gy, the release was even stronger, reaching the maximum earlier (at 48 h, 11.09 x 10(3) AU, range 6.89-18.28 x 10(3) AU). In non-irradiated EPLC, nucleosomes constantly increased slightly. At 10 Gy, we observed a considerably higher release of nucleosomes in EPLC, with a maximum at 72 h (before irradiation: 2.79 x 10(3) AU, range 2.42-3.80 x 10(3) AU, and after 72 h: 7.16 x 10(3) AU, range 4.30-16.20 x 10(3) AU), which was more than 3.5 times higher than in BEAS-2B. At 30 Gy, the maximum (6.22 x 10(3) AU, range 5.13-9.71 x 10(3) AU) was observed already after 24 h. These results indicate that normal bronchoepithelial and malignant lung cancer cells contribute to the release of nucleosomes during irradiation in a dose-and time-dependent manner with cancer cells having a stronger impact at low doses. Copyright (C) 2004 S. Karger AG, Basel