Background: Pentraxins (PTX) play key roles in innate immunity and inflammatory responses. An increase in PTX3 levels may be a marker of early radiation injury in the lung. Thus, we aimed to determine the effect of radiation on PTX3 expression in a lung injury mouse model. Materials and Methods: Twenty-four 6–8-week-old mice were divided into 4 groups, one control (group 1) and three experimental groups (groups 2–4) irradiated with 6 MV photons and 5 Gy in a single fraction. Groups 2, 3, and 4 were sedated and euthanized 24, 72, and 168 h after radiation, respectively. The right lung middle lobe was then removed for histochemical examination and immunostaining for PTX3 expression, which was evaluated semi-quantitatively using H-SCORE analysis. Kolmogorov-Smirnov and Kruskal Wallis one-way analysis of variance were used for statistical analysis. Results: Immunohistochemistry of lung tissue samples showed different PTX3 expression levels across the four groups. Group 1 showed weak staining (232.50 ± 9.501), while group 2 (301.50 ± 7.472) and group 3 (283.50 ± 7.090) showed strong immunoreactivity. Group 4 showed moderate PTX3 immunoreactivity (271.50 ± 10.013). Moreover, H-score values between control and early radiation groups were statistically significant (group 1 vs. group 2, p < 0.001; group 1 vs. group 3, p = 0.002). Conclusion: PTX3 levels may be an early marker for long-term radiation effects. Our study provides insights into the pathological processes of pulmonary inflammation and acute radiation injury, and may provide novel therapeutic strategies for controlling pulmonary inflammation without eliciting radiation injury.

Background: Adrenomedullin (AM) and its receptor, receptor activity-modifying protein (RAMP) 2 have pleiotropic regulatory functions in normal tissue and cancer tissue. AM is produced and secreted both numerous stromal cells and tumor cells. This study aims to investigate a possible role of AM and RAMP2 in the radiation exposure in the normal lung tissue. Materials and Methods: Four groups with 6 male adult Swiss Albino mice per group were investigated. The mice were subjected to a 500 cGy single-dose radiation exposure in the total body radiation device and lung tissues were collected. 1, 2, and 7 days after radiation exposure, with 1 reference group which was not exposed to radiation. Results: The general histology and the immunohistochemistry of the tissue samples prepared with anti- AM, anti–RAMP2, and monoclonal antibodies were investigated, yielding a statistically significant increase for AM on day 3 and for RAMP2 on day 1 after radiation exposure. Conclusion: The observed increase of AM and RAMP2 concentrations in the normal tissue matrix after radiation exposure may play a role in the side effects of radiotherapy. 

Background: Non-small cell lung cancer (NSCLC) is the most commonly diagnosed cancer, and radiotherapy (RT) is used for the cancer therapy. RT affects DNA and causes DNA double-strand breaks which are repaired by DNA repair protein ataxia telangiectasia mutated (ATM). RT also affects the mitochondria which is a key player in mediating the radiation response in tumors and removing damaged mitochondria through mitophagy. During mitophagy, PARKIN accumulates on defective mitochondria to mediate the clearance of damaged mitochondria. This study examines the effect of radiation on mitophagy using PARKIN and ATM antibodies on the human NSCLC A549 line. Materials and Methods: A549 cells were treated with 2, 4, 6 and 8 Gy of radiation were analyzed on days 1 and 3 after a single dose of radiotherapy. PARKIN and ATM expressions of A549 cells were examined by using immunohistochemical technique. Results: In the control groups, weak immunoreactivity of ATM and PARKIN was observed on both days 1 and 3.  The most intense ATM expression was seen in the 6 and 8 Gy groups after day 1. The most intense PARKIN expression was seen after the days 1 and 3 in the 2 Gy groups. PARKIN immunoreactivity decreased due to increasing radiation dose. Conclusion: It must be considered that mitophagy mechanisms are activated in RT applications. It must be considered that the activation of mitophagy mechanisms in RT and A549 lung cancer cell lines may provide hemostasis in cancer cells. Molecules targeting mitophagy must be developed for use with radiotherapy.