Abstract
We measured number of bcl-2, apoptotic, neutrophil, and surfactant apoprotein D (SP-D) positive cells in irradiated rat lungs during different time points after the sublethal whole-thorax irradiation of rats. We also investigated the influence of pentoxifylline (PTX) therapy on these markers. Wistar rats were given 15 Gy thoracic irradiation and PTX (35 mg/kg) twice a week. Animals were examined histologically and imunohistochemically at intervals from 1-12 weeks. In non-treated rats compared with treated rats, bcl-2 expression was significantly inhibited from 4 weeks after irradiation. A higher apoptosis presence in non-treated rats from 4 weeks was found and apoptosis development in PTX-treated animals was delayed and started 8 weeks after irradiation. Similar differences were measured during neutrophil granulocytes examination. Neutrophil penetration in non-treated rats was found 5 weeks after irradiation in contrast to the RP onset of PTX-treated animals 8 weeks after irradiation. The number of SP-D positive cells in non-treated rats observed until 5 weeks after irradiation was higher than in the control group. PTX-treated animals expressed higher number of SP-D positive cells during the whole experiment than the control group. We suggest that apoptosis is linked to neutrophil granulocyte actions during the RP onset and that PTX-therapy causes diminished inflammation development.
Highlights
Radiation pneumonitis (RP) is defined as an exudative inflammation which occurs as a result of ionizing radiation [5] and it is considered as an alveolitis resulting from damage to pneumocytes and the endothelial cells [13]
We investigated apoptosis by the caspase cleavage product of cytokeratin 18 as well as the number of neutrophils and surfactant apoprotein D positive cells in the irradiated lungs by computer image analysis
In diffuse alveolar damage (DAD), the absence of bcl-2 expression in type IIpneumocytes suggest that these cells are vulnerable to the effects of free radical-induced apoptosis [14]
Summary
Radiation pneumonitis (RP) is defined as an exudative inflammation which occurs as a result of ionizing radiation [5] and it is considered as an alveolitis resulting from damage to pneumocytes and the endothelial cells [13]. This condition is termed adult respiratory distress syndrome (ARDS), sometimes as diffuse alveolar damage (DAD; 16). Fuks et al [8] first described apoptosis in irradiated lung tissue by the DNA terminal transferase nick-end translation method This method revealed time and dose-dependent apoptosis mainly in endothelial and mesothelial cells at 1 week after irradiation
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