Chitkara College of Pharmacy, Chitkara University, Punjab, Chandigarh, India.
Department of Biology, Faculty of Science, Selcuk University Campus, Konya, Turkey.
Curr Neuropharmacol. 2022;20(2):324-343. doi: 10.2174/1570159X19666210524152817.
Ionizing radiation from telluric sources is unceasingly an unprotected pitfall to humans. Thus, the foremost contributors to human exposure are global and medical radiations. Various evidences assembled during preceding years reveal the pertinent role of ionizing radiation- induced oxidative stress in the progression of neurodegenerative insults, such as Parkinson's disease, which have been contributing to increased proliferation and generation of reactive oxygen species.
This review delineates the role of ionizing radiation-induced oxidative stress in Parkinson's disease and proposes novel therapeutic interventions of flavonoid family, offering effective management and slowing down the progression of Parkinson's disease.
Published papers were searched in MEDLINE, PubMed, etc., published to date for indepth database collection.
The oxidative damage may harm the non-targeted cells. It can also modulate the functions of the central nervous system, such as protein misfolding, mitochondria dysfunction, increased levels of oxidized lipids, and dopaminergic cell death, which accelerate the progression of Parkinson's disease at the molecular, cellular, or tissue levels. In Parkinson's disease, reactive oxygen species exacerbate the production of nitric oxides and superoxides by activated microglia, rendering death of dopaminergic neuronal cell through different mechanisms.
Rising interest has extensively engrossed in the clinical trial designs based on the plant-derived family of antioxidants. They are known to exert multifarious impact on neuroprotection via directly suppressing ionizing radiation-induced oxidative stress and reactive oxygen species production or indirectly increasing the dopamine levels and activating the glial cells.
来自地球的电离辐射是人类持续面临的一种无保护的隐患。因此，人类接触的主要辐射源是全球性和医疗辐射。近年来积累的各种证据表明，电离辐射诱导的氧化应激在神经退行性损伤（如帕金森病）的进展中起着重要作用，这些损伤会导致活性氧的增殖和产生增加。
本综述阐述了电离辐射诱导的氧化应激在帕金森病中的作用，并提出了黄酮类化合物家族的新的治疗干预措施，为帕金森病的有效管理和减缓其进展提供了新的思路。
在 MEDLINE、PubMed 等数据库中搜索已发表的论文，以获取最新的深入数据库收集信息。
氧化损伤可能会损害非靶向细胞。它还可以调节中枢神经系统的功能，如蛋白质错误折叠、线粒体功能障碍、氧化脂质水平升高和多巴胺能神经元死亡，这些都会在分子、细胞或组织水平上加速帕金森病的进展。在帕金森病中，活性氧会加剧激活的小胶质细胞产生的一氧化氮和超氧化物，通过不同的机制导致多巴胺能神经元细胞死亡。
基于植物源性抗氧化剂家族的临床试验设计引起了广泛的关注。它们通过直接抑制电离辐射诱导的氧化应激和活性氧的产生，或间接增加多巴胺水平和激活神经胶质细胞，对神经保护产生多种影响。
