Cancers · 2025
Daily Consumption of Apigenin Prevents Acute Lymphoma/Lymphoblastic Leukemia in Male C57BL/6J Mice Exposed to Space-like Radiation.
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Peanlikhit Tanat, Liu Jingxuan, Ahmed Tahmeena, Welsh James S, Karakach Tobias, Shroyer Kenneth R, Whorton Elbert, Rithidech Kanokporn Noy
Аннотация
INTRODUCTION: The work presented here is part of our study series aimed at investigating the countermeasure effectiveness of apigenin (AP) against both early and late effects of heavy silicon (28Si) on the same cohort of exposed male C57BL/6 mice. We previously reported the countermeasure of AP against 28Si-induced early effects of 28Si ions. This section focuses on the protective effects of AP on late effects, specifically on the induction of acute lymphoma/lymphoblastic leukemia.
METHOD: Mice received a diet containing 20 mg/kg body weight of AP for five days before and after total-body irradiation with either 0 or 0.5 Gy of 260 MeV 28Si ions. They were divided into four groups based on AP intake and irradiation status. At one-week after irradiation, six mice from each group were euthanized to assess AP's effectiveness against early inflammation (in the bone marrow and gut tissues) and gut dysbiosis. The remaining mice were monitored until approximately 770 days of age. Incidence rates were analyzed using Chi-Square tests, while survival data were evaluated with Kaplan-Meier plots and log-rank tests, setting significance at p ≤ 0.05.
RESULTS: At 770 days, survival rates were 37% for 28Si-exposed mice and 63% for those consuming AP, despite irradiation. There was a 2.57-fold increase in acute lymphoma/lymphoblastic leukemia incidence among 28Si-exposed mice not receiving AP compared to controls and AP-fed mice. Together with our previous report on the countermeasure activity of AP against early effects, these findings suggest that the gut-bone marrow axis plays an important role in 28Si-induced acute lymphoma/lymphoblastic leukemia.
CONCLUSION: Our findings demonstrate that AP is an effective means of tackling the challenges posed by space radiation, and it has the potential to revolutionize protection in this critical area.
METHOD: Mice received a diet containing 20 mg/kg body weight of AP for five days before and after total-body irradiation with either 0 or 0.5 Gy of 260 MeV 28Si ions. They were divided into four groups based on AP intake and irradiation status. At one-week after irradiation, six mice from each group were euthanized to assess AP's effectiveness against early inflammation (in the bone marrow and gut tissues) and gut dysbiosis. The remaining mice were monitored until approximately 770 days of age. Incidence rates were analyzed using Chi-Square tests, while survival data were evaluated with Kaplan-Meier plots and log-rank tests, setting significance at p ≤ 0.05.
RESULTS: At 770 days, survival rates were 37% for 28Si-exposed mice and 63% for those consuming AP, despite irradiation. There was a 2.57-fold increase in acute lymphoma/lymphoblastic leukemia incidence among 28Si-exposed mice not receiving AP compared to controls and AP-fed mice. Together with our previous report on the countermeasure activity of AP against early effects, these findings suggest that the gut-bone marrow axis plays an important role in 28Si-induced acute lymphoma/lymphoblastic leukemia.
CONCLUSION: Our findings demonstrate that AP is an effective means of tackling the challenges posed by space radiation, and it has the potential to revolutionize protection in this critical area.