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<p>The blood system is sensitive to radiation, making it vulnerable to damage. Diallyl disulfide (DADS), a&#xa0;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&#xa0;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&#xa0;protective effect on the radiation damage to the blood system. Our findings underscore the potential of DADS as a&#xa0;protective agent against radiation-induced damage to the blood system.</p>

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

  • 期刊论文

  • 发表日期：

    2026年4月8日

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

摘要

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.