Nam Seon Young, Jeong Haemin
R&D Strategy & Planning Section, Radiation Health Institute, Korea Hydro & Nuclear Power Co. Ltd., Seoul, Republic of Korea.
Research & Development Team, PeopleBio, Seongnam-si, Republic of Korea.
Int J Radiat Biol. 2025;101(8):876-886. doi: 10.1080/09553002.2025.2502018. Epub 2025 Jun 26.
To investigate the biological effects of low-dose ionizing radiation (LDIR) on living organisms, we analyzed the effects of LDIR of 0.05 Gy and its mechanism on the which is an ideal model organism for aging studies due to its short lifespan and conserved molecular pathways.
The embryos of were irradiated and we analyzed the effects of LDIR treatment on the lifespan of . To investigate the effects of LDIR under oxidative stress conditions, because oxidative stress is a major cause of aging, reactive oxygen species (ROS) levels and the oxidative stress susceptibility of flies under hydrogen peroxide (HO)-induced oxidative stress conditions were evaluated at early post-irradiation time points. We next elucidated the effects of LDIR on the molecular mechanisms of lifespan extension.
LDIR extended the lifespan, but did not alter developmental rates. In addition, the locomotive deterioration of aged flies was rescued by exposure to a 0.05 Gy dose of γ-irradiation. LDIR increased the survival rates and locomotive ability under oxidative stress conditions and decreased mRNA levels of the pro-apoptotic factors, and . Moreover, 0.05 Gy of LDIR decreased ROS accumulation and increased superoxide dismutase (SOD) activity in flies exposed to HO. Also, LDIR activated AKT pathway in HO-treated flies and inhibition of AKT activity suppressed the effects of LDIR.
LDIR of 0.05 Gy extends the lifespan and survival rates under HO-induced oxidative stress conditions by controlling ROS levels via AKT activation.
为了研究低剂量电离辐射（LDIR）对生物体的生物学效应，我们分析了0.05 Gy的LDIR对[具体生物名称未给出]的影响及其机制，[具体生物名称未给出]因其寿命短和分子途径保守，是衰老研究的理想模式生物。
对[具体生物名称未给出]的胚胎进行辐射，并分析LDIR处理对[具体生物名称未给出]寿命的影响。由于氧化应激是衰老的主要原因，为了研究氧化应激条件下LDIR的影响，在辐射后早期时间点评估了过氧化氢（HO）诱导的氧化应激条件下果蝇的活性氧（ROS）水平和氧化应激敏感性。接下来，我们阐明了LDIR对寿命延长分子机制的影响。
LDIR延长了寿命，但未改变发育速率。此外，暴露于0.05 Gy剂量的γ辐射可挽救老年果蝇的运动能力衰退。在氧化应激条件下，LDIR提高了存活率和运动能力，并降低了促凋亡因子[具体因子未给出]和[具体因子未给出]的mRNA水平。此外，0.05 Gy的LDIR减少了暴露于HO的果蝇中的ROS积累，并增加了超氧化物歧化酶（SOD）活性。而且，LDIR激活了HO处理果蝇中的AKT途径，抑制AKT活性则抑制了LDIR的作用。
0.05 Gy的LDIR通过激活AKT来控制ROS水平，从而在HO诱导的氧化应激条件下延长寿命和提高存活率。
