Mechanism of Genome Damage Response Induced by Ultrasoun

一个可能的候选过程涉及声化学活性，其中活性氧介导dna单链断裂的产生。然而，在这里，我们提供了令人信服的新证据，强烈支持纯机械机制。此外，通过特异性试验（中性彗星尾和γ - h2ax灶形成染色）的组合，我们首次证明，即使中等强度的US暴露也会显示DNA双链断裂，通过其设施在多个癌细胞系中产生DNA损伤。值得注意的是，共定位分析强调，电离辐射和超声对各自的γ - h2ax病灶形成模式具有明显不同的特征，这可能反映了引发损伤形成的不同应力分布。

A likely candidate process has been suggested to involve sonochemical activity, where reactive oxygen species mediate the generation of DNAsingle-strand breaks. Here however, we provide compelling new evidence that strongly supports a purely mechanical mechanism. Moreover, by a combination of specific assays （neutral comet tail and staining for γH2AX foci formation) we demonstrate for the first time that US exposure at even moderate intensities exhibits DNAdouble-strand breaks, through its facility to generate DNA damage across multiple cancer lines. Notably, colocalization assays highlight that ionizing radiation and ultrasound have distinctly different signatures to their respective γH2AX foci formation patterns, likely reflecting the different stress distributions that initiated damage formation.