Abstract：
Organisms frequently suffer negative effects from large doses of ionizing radiation. However, radiation is not as hazardous at lower doses as was once believed. The current study aims to evaluate the possible radio-adaptive effect induced by low-dose radiation (LDR) in modulating high-dose radiation (HDR) and N-nitrosodiethylamine (NDEA)-induced lung injury in male albino rats. Sixty-four male rats were randomly divided into four groups: Group 1 (control): normal rats; Group 2 (D): rats given NDEA in drinking water; Group 3 (DR): rats administered with NDEA then exposed to fractionated HDR; and Group 4 (DRL): rats administered with NDEA then exposed to LDR + HDR. In the next stage, malondialdehyde (MDA), glutathione reduced (GSH), catalase (CAT), and superoxide dismutase (SOD) levels in the lung tissues were measured. Furthermore, the enzyme-linked immunoassay analysis technique was performed to assess the Toll-like receptor 4 (TLR4), interleukin-1 receptor-associated kinase 4 (IRAK4), and mitogen-activated protein kinases (MAPK) expression levels. Histopathological and DNA fragmentation analyses in lung tissue, in addition to hematological and apoptosis analyses of the blood samples, were also conducted. Results demonstrated a significant increase in antioxidant defense and a reduction in MDA levels were observed in LDR-treated animals compared to the D and DR groups. Additionally, exposure to LDR decreased TLR4, IRAK4, and MAPK levels, decreased apoptosis, and restored all the alterations in the histopathological, hematological parameters, and DNA fragmentation, indicating its protective effects on the lung when compared with untreated rats. Taken together, LDR shows protective action against the negative effects of subsequent HDR and NDEA. This impact may be attributable to the adaptive response induced by LDR, which decreases DNA damage in lung tissue and activates the antioxidative, antiapoptotic, and anti-inflammatory systems in the affected animals, enabling them to withstand the following HDR exposure.
摘要：
生物体经常遭受大剂量电离辐射的负面影响。然而,辐射在较低剂量下并不像人们曾经认为的那样危险。本研究旨在评估低剂量辐射（LDR）在调节雄性白化病大鼠高剂量辐射（HDR）和N-亚硝基二乙胺（NDEA）诱导的肺损伤中可能引起的放射适应性效应。将64只雄性大鼠随机分为四组：第1组（对照）：正常大鼠；第2组（D）：在饮用水中给予NDEA的大鼠；第3组（DR）：给予NDEA的大鼠，然后暴露于分级HDR；第4组（DRL）：给予NDEA的大鼠，然后暴露于LDRHDR。在下一阶段,丙二醛（MDA），还原型谷胱甘肽（GSH），过氧化氢酶(CAT),测定肺组织中超氧化物歧化酶(SOD)的含量。此外，进行酶联免疫分析技术以评估Toll样受体4（TLR4），白细胞介素-1受体相关激酶4（IRAK4），和丝裂原活化蛋白激酶（MAPK）表达水平。肺组织的组织病理学和DNA片段分析，除了血液样本的血液学和细胞凋亡分析，也进行了。结果表明,与D和DR组相比,在LDR处理的动物中观察到抗氧化剂防御的显著增加和MDA水平的降低。此外,暴露于LDR会降低TLR4，IRAK4和MAPK水平，细胞凋亡减少，恢复了组织病理学的所有改变，血液学参数,和DNA片段化,表明与未治疗的大鼠相比，其对肺的保护作用。一起来看,LDR显示针对随后的HDR和NDEA的负面影响的保护作用。这种影响可能归因于LDR诱导的适应性反应，减少肺组织中的DNA损伤并激活抗氧化剂，抗凋亡，和受影响动物的抗炎系统，使他们能够承受以下HDR曝光。
