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DOI 10.1007/s00066-026-02517-0

Медицинская библиотека · Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2026

Diallyl disulfide reduces oxidative stress to mitigate uranium tailings radiation-induced damage to the hematopoietic system.

Wei Yuanyun, Li Linwei, Li Yuanyuan, Wang Qingyu, Gong Yaqi, Wei Shuang, Yi Fang, Guo Caimao, Wu Wenyu, Yu Yueqiu, Lin Xiang, Kuang Ye, Qin Hui, Yi Lan

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Аннотация

The blood system is sensitive to radiation, making it vulnerable to damage. Diallyl disulfide (DADS), a primary bioactive compound derived from allicin degradation, has shown significant potential in tumor prevention and treatment. This study investigates the role and mechanisms of DADS in mitigating radiation-induced damage to the blood system, thereby providing both experimental evidence and theoretical insights for further research on radiation damage protection. A C57BL/6J mouse model was exposed to low-dose ionizing radiation and treated with DADS; spleen red pulp area, bone marrow morphology, peripheral blood indices, and erythropoietin levels were addressed. In addition, a GM12878 human B lymphocyte cell model was used to evaluate the effects of DADS on cell viability and apoptosis during irradiation. Our results show that DADS reduces radiation-induced damage both in mouse and GM12878 cell models. Specifically, DADS shields GM12878 cell apoptosis from radiation by reducing reactive oxygen species (ROS) production, thereby exerting a protective effect on the radiation damage to the blood system. Our findings underscore the potential of DADS as a protective agent against radiation-induced damage to the blood system.

Для цитирования: Wei Yuanyun, Li Linwei, Li Yuanyuan, Wang Qingyu, Gong Yaqi, Wei Shuang, Yi Fang, Guo Caimao, Wu Wenyu, Yu Yueqiu, Lin Xiang, Kuang Ye, Qin Hui, Yi Lan. Diallyl disulfide reduces oxidative stress to mitigate uranium tailings radiation-induced damage to the hematopoietic system.. Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al]. 2026. DOI: 10.1007/s00066-026-02517-0.
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