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. Author manuscript; available in PMC: 2023 Jun 1.
Published in final edited form as: Radiat Res. 2022 Jun 1;197(6):569–582. doi: 10.1667/RADE-21-00181.1

FIG. 7.

FIG. 7.

Proposed model of the mitochondria-driven mechanisms by which proton-FLASH irradiation can significantly protect the mitochondria from damage including mitochondrial morphology and function via the p53-Drp1 pathway. Exposure of normal cells to conventional-dose protons can make p-Drp1 undergo dephosphorylation with consequent Drp1 translocation into the mitochondria, which may eventually lead to mitochondrion damage and cell death. In contrast, p-Drp1 protein level does not significantly change after exposure to similar proton doses delivered using FLASH-RT. As opposed to protons delivered using FLASH-RT, CONV-RT stimulates the cytoplasmic localization of Drp1 to mitochondria resulting in their dysfunction and fragmentation.