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辐射诱导的旁观者效应:迷迭香酸在体内和体外辐射防护能力的丧失

Radiation-Induced Bystander Effect: Loss of Radioprotective Capacity of Rosmarinic Acid In Vivo and In Vitro.

作者信息

Olivares Amparo, Alcaraz-Saura Miguel, Achel Daniel Gyingiri, Berná-Mestre Juan de Dios, Alcaraz Miguel

机构信息

Radiology and Physical Medicine Department, School of Medicine, University of Murcia, 30100 Murcia, Spain.

Applied Radiation Biology Centre, Radiological and Medical Sciences Research Institute, Ghana Atomic Energy Commission, Legon-Accra GE-257-0465, Ghana.

出版信息

Antioxidants (Basel). 2021 Feb 3;10(2):231. doi: 10.3390/antiox10020231.

Abstract

In radiation oncology, the modulation of the bystander effect is a target both for the destruction of tumor cells and to protect healthy cells. With this objective, we determine whether the radioprotective capacity of rosmarinic acid (RA) can affect the intensity of these effects. Genoprotective capacity was obtained by determining the micronuclei frequencies in in vivo and in vitro assays and the cell survival was determined by the (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay) (MTT) assay in three cell lines (PNT2, TRAMPC1 and B16F10), both in direct exposure to X-rays and after the production of radiation-induced bystander effect. The administration of RA in irradiated cells produced a decrease in the frequency of micronuclei both in vivo and in vitro, and an increase in cell survival, as expression of its radioprotective effect ( < 0.001) attributable to its ability to scavenge radio-induced free radicals (ROS). However, RA does not achieve any modification in the animals receiving serum or in the cultures treated with the irradiated medium, which expresses an absence of radioprotective capacity. The results suggest that ROS participates in the formation of signals in directly irradiated cells, but only certain subtypes of ROS, the cytotoxic products of lipid peroxidation, participate in the creation of lesions in recipient cells.

摘要

在放射肿瘤学中,调节旁观者效应既是破坏肿瘤细胞的目标,也是保护健康细胞的目标。出于这一目的,我们确定迷迭香酸(RA)的辐射防护能力是否会影响这些效应的强度。通过在体内和体外试验中测定微核频率来获得基因保护能力,并通过(3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐法)(MTT)法在三种细胞系(PNT2、TRAMPC1和B16F10)中测定细胞存活率,包括直接暴露于X射线时以及产生辐射诱导的旁观者效应之后。在受辐照细胞中给予RA会使体内和体外的微核频率降低,并使细胞存活率增加,这体现了其辐射防护作用(<0.001),这归因于其清除辐射诱导的自由基(ROS)的能力。然而,RA在接受血清的动物或用辐照培养基处理的培养物中并未产生任何改变,这表明其缺乏辐射防护能力。结果表明,ROS参与直接受辐照细胞中信号的形成,但只有某些亚型的ROS,即脂质过氧化的细胞毒性产物,参与受体细胞中损伤的产生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/471e/7913630/ed8631f3da56/antioxidants-10-00231-g001.jpg

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