Early-life atomic-bomb irradiation accelerates immunological aging and elevates immune-related intracellular reactive oxygen species

早期原子弹辐射会加速免疫衰老并提高免疫相关细胞内活性氧的水平。

阅读:1

Abstract

Reactive oxygen species (ROS) play an important role in immune responses; however, their excessive production and accumulation increases the risk of inflammation-related diseases. Although irradiation is known to accelerate immunological aging, the underlying mechanism is still unclear. To determine the possible involvement of ROS in this mechanism, we examined 10,023 samples obtained from 3752 atomic-bomb survivors in Hiroshima and Nagasaki, who participated in repeated biennial examinations from 2008 to 2016, for the effects of aging and radiation exposure on intracellular ROS (H(2) O(2) and O(2) (•-) ) levels, percentages of T-cell subsets, and the effects of radiation exposure on the relationship between cell percentages and intracellular ROS levels in T-cell subsets. The cell percentages and intracellular ROS levels in T-cell subsets were measured using flow cytometry, with both fluorescently labeled antibodies and the fluorescent reagents, carboxy-DCFDA and hydroethidine. The percentages of naïve CD4(+) and CD8(+) T cells decreased with increasing age and radiation dose, while the intracellular O(2) (•-) levels in central and effector memory CD8(+) T cells increased. Additionally, when divided into three groups based on the percentages of naïve CD4(+) T cells, intracellular O(2) (•-) levels of central and effector memory CD8(+) T cells were significantly elevated with the lowest radiation dose group in the naïve CD4(+) T cells. Thus, the radiation exposure-induced decrease in the naïve CD4(+) T cell pool size may reflect decreased immune function, resulting in increased intracellular ROS levels in central and effector memory CD8(+) T cells, and increased intracellular oxidative stress.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。