Evaluating Superoxide Dismutase (SOD), Glutathione (GSH), Malondialdehyde (MDA) and the Histological Changes of the Lung Tissue after γ-Irradiation in Rats

Background & Objective: The lung is a radiosensitive organ and its damage is a dose-limiting factor in radiotherapy. Different side effects such as pneumonia and lung fibrosis are found in patients with thorax irradiation. The objective of the present study is to evaluate the effects of &gamma;-irradiation on acute and chronic injuries of lung tissue in rats. Materials & Methods: 32 rats were divided into two groups. Control group consisted of 14 rats that underwent shame irradiation. In radiation group, 18 rats underwent &gamma;-irradiation. The rats were exposed to &gamma;-irradiation 18 Gy using a single fraction cobalt-60 unit. Eight rats in each group were sacrificed 24 hours after radiotherapy for determining Superoxide Dismutase (SOD), Glutathione (GSH), Malondialdehyde (MDA), and histopathological evaluations. Remained animals were sacrificed eight weeks after radiotherapy for histopathological evaluation. Results: Compared to control group, the level of SOD and GSH significantly decreased and MDA level significantly increased in radiation group 24 hours following irradiation, (p=0.001, p<0.001, p=0.001) respectively. Early histopathological results after 24 hours showed that radiation increases neutrophil, macrophage, and inflammation incidence compared to control group (p<0.05). Late histopathological evaluation after eight weeks revealed significant increase in factors including mast cells, pulmonary edema, vascular thickness, vascular damage, and also inflammation and fibrosis incidence in case group compared to radiation group &nbsp;(p<0.05). Conclusion: Localized chest radiation with dose of 18 Gy induces changes in oxidative stress indices and histopathological lung tissue damage in short and long term

The role of rectal sparing devices in post-prostatectomy radiotherapy: a review article

Adjuvant or salvage radiotherapy can control biochemical relapse after radical prostatectomy and reduce the risk of distant metastases. Dose-escalated radiotherapy after radical prostatectomy can lead to improved biochemical relapse-free survival. Over the last decades, despite the technological advancements in prostate radiotherapy, radiation-induced rectal toxicity is still the main limiting factor for dose escalation owing to the anatomical proximity of the prostate gland to the rectum. To this end, several rectal sparing devices, including Endorectal balloons (ERBs), prostate-rectum spacers (e.g. SpaceOAR hydrogel), and rectal retractor have been explored to increase the distance between the prostate and the rectum to reduce rectal radiation doses and toxicities. Over the last decade, several studies applied these devices during post-prostatectomy radiotherapy setting. Therefore, the purpose of this review is to evaluate the impact of rectal sparing devices on dose-volume parameters of anorectal, radiation-induced rectal toxicity, and prostate bed motion during post-prostatectomy radiotherapy. The results showed that although using ERBs can lead to stability in the target volume position, it cannot reduce rectal radiation doses, in particular dose to the anterior rectal wall. The application of ERBs can reduce the received dose of the anal wall and increase the geometric reproducibility of the clinical target volume (CTV) position. However, the role of ERBs in reducing the received dose of the rectal wall is still controversial, which can be associated with the displacement of the anterior rectal wall towards the prostate bed (high radiation dose area). The use of SpaceOAR hydrogel can significantly increase the distance between the rectum and the prostate bed and ultimately reduce the dose received by the rectal wall. Also, the use of rectal retractor remarkably reduces rectal radiation doses. The dosimetric and clinical results of the use of SpaceOAR hydrogel and rectal retractor are very promising, and these devices can be used for patients after the necessary evaluations by radiation oncologist in post-prostatectomy radiotherapy. However, further studies will be required to elucidate the efficacy of SpaceOAR hydrogel and rectal retractor in reducing radiotherapy-induced rectal toxicity following post-prostatectomy radiotherapy. Keywords: prostatectomy, prostate cancer, radiotherapy, rectum

Radioprotective effects of hesperidin on oxidative damages and histopathological changes induced by X-irradiation in rats heart tissue

This study was carried out to evaluate radioprotective effects of hesperidin (HES) administration before the irradiation on the cardiac oxidative stress and histopathological changes in an experimental rat model. The cardiovascular complications of radiation exposure cause morbidity and mortality in patients who received radiotherapy. HES, an antioxidant flavonoid found in citrus fruits, suggests the protection against the tissue damage. Fifty-eight rats were divided into four groups: Group 1 received phosphate buffered saline (PBS) and sham radiation; Group 2, HES and sham radiation; Group 3, PBS and radiation; and Group 4, HES and radiation. The rats were exposed to single dose of 18 Gy of 6 MV X-ray. One hundred milligrams per kilogram doses of HES was administered for 7 days before irradiation. The estimation of superoxide dismutase (SOD), malondialdehyde (MDA), and histopathological analyses was performed at 24 h and 8 weeks after radiation exposure. The irradiation of chest area resulted in an elevated MDA level and decreased SOD activity. Moreover, long-term pathological lesions of radiation were inflammation, fibrosis, the increased number of mast cells and macrophages, and development of plaque, vascular leakage, myocardial degeneration, and myocyte necrosis. Although the administration of HES decreases inflammation, fibrosis, mast cell and macrophage numbers, and myocyte necrosis, it did not result in reduced thrombus, myocardium degeneration, and vascular leakage. In conclusion, these results suggest that HES can perform a radioprotection action. The protective effect of HES may be attributable to its immunomodulatory effects and free radical-scavenging properties

Hesperidin as radioprotector against radiation-induced lung damage in rat: A histopathological study

Reactive oxygen species (ROS) are generated by ionizing radiation, and one of the organs commonly affected by ROS is the lung. Radiation-induced lung injury including pneumonia and lung fibrosis is a dose-limiting factor in radiotherapy (RT) of patients with thorax irradiation. Administration of antioxidants has been proved to protect against ROS. The present study was aimed to assess the protective effect of hesperidin (HES) against radiation-induced lung injury of male rats. Fifty rats were divided into three groups. G1: Received no HES and radiation (sham). G2: Underwent γ-irradiation to the thorax. G3: Received HES and underwent γ-irradiation. The rats were exposed to a single dose of 18 Gy using cobalt-60 unit and were administered HES (100 mg/kg) for 7 days before irradiation. Histopathological analysis was performed 24 h and 8 weeks after RT. Histopathological results in 24 h showed radiation-induced inflammation and presence of more inflammatory cells as compared to G1 (P < 0.05). Administration of HES significantly decreased such an effect when compared to G2 (P < 0.05). Histopathological evaluation in 8 weeks showed a significant increase in mast cells, inflammation, inflammatory cells, alveolar thickness, vascular thickness, pulmonary edema, and fibrosis in G2 when compared to G1 (P < 0.05). HES significantly decreased inflammatory response, fibrosis, and mast cells when compared to G2 (P < 0.05). Administration of HES resulted in decreased radiation pneumonitis and radiation fibrosis in the lung tissue. Thus, the present study showed HES to be an efficient radioprotector against radiation-induced damage in the lung of tissue rats

Mitigation of Radiation-Induced Lung Pneumonitis and Fibrosis Using Metformin and Melatonin: A Histopathological Study

Background and objectives: Pneumonitis and fibrosis are the most common consequences of lung exposure to a high dose of ionizing radiation during an accidental radiological or nuclear event, and may lead to death, after some months to years. So far, some anti-inflammatory and antioxidant agents have been used for mitigation of lung injury. In the present study, we aimed to detect possible mitigatory effects of melatonin and metformin on radiation-induced pneumonitis and lung fibrosis. Materials and methods: 40 male mice were divided into 4 groups (10 mice in each). For control group, mice did not receive radiation or drugs. In group 2, mice were irradiated to chest area with 18 Gy gamma rays. In groups 3 and 4, mice were first irradiated similar to group 2. After 24 h, treatment with melatonin as well as metformin began. Mice were sacrificed after 100 days for determination of mitigation of lung pneumonitis and fibrosis by melatonin or metformin. Results: Results showed that both melatonin and metformin are able to mitigate pneumonitis and fibrosis markers such as infiltration of inflammatory cells, edema, vascular and alveolar thickening, as well as collagen deposition. Conclusion: Melatonin and metformin may have some interesting properties for mitigation of radiation pneumonitis and fibrosis after an accidental radiation event

Radiation-induced inflammation and autoimmune diseases

Abstract Currently, ionizing radiation (IR) plays a key role in the agricultural and medical industry, while accidental exposure resulting from leakage of radioactive sources or radiological terrorism is a serious concern. Exposure to IR has various detrimental effects on normal tissues. Although an increased risk of carcinogenesis is the best-known long-term consequence of IR, evidence has shown that other diseases, particularly diseases related to inflammation, are common disorders among irradiated people. Autoimmune disorders are among the various types of immune diseases that have been investigated among exposed people. Thyroid diseases and diabetes are two autoimmune diseases potentially induced by IR. However, the precise mechanisms of IR-induced thyroid diseases and diabetes remain to be elucidated, and several studies have shown that chronic increased levels of inflammatory cytokines after exposure play a pivotal role. Thus, cytokines, including interleukin-1(IL-1), tumor necrosis factor (TNF-α) and interferon gamma (IFN-γ), play a key role in chronic oxidative damage following exposure to IR. Additionally, these cytokines change the secretion of insulin and thyroid-stimulating hormone(TSH). It is likely that the management of inflammation and oxidative damage is one of the best strategies for the amelioration of these diseases after a radiological or nuclear disaster. In the present study, we reviewed the evidence of radiation-induced diabetes and thyroid diseases, as well as the potential roles of inflammatory responses. In addition, we proposed that the mitigation of inflammatory and oxidative damage markers after exposure to IR may reduce the incidence of these diseases among individuals exposed to radiation