抄録
Ultrasound (US) is indispensable for most medical fields: US at very low intensities is used for clinical diagnosis; high intensity focused US is used for thermal ablation of tumors; and non-thermal low-intensity US is being tested for its potential in cancer therapy. Low-intensity US has been shown to induce cell death in cancer cells; however, the underlying mechanism remains elusive. US effects have been thought to result from the stresses through cavitation microbubbles/their collapse-associated liquid jets and through production of reactive oxygen species (ROS). Previous studies implicated the importance of ROS-mediated DNA single-strand breaks (SSBs) in US-induced cell death. However, this perspective is questionable because numerous SSBs induced by ROS lead to no/few double-strand breaks (DSBs), the most cytotoxic damage to cell nucleus. Here, we describe novel evidence that US induces DSBs in human leukemia cells via mechanical effects of cavitation, but not free radicals produced by sonochemical actions.
