An investigation on the mechanism(s) behind sonodynamic therapy and the use of sonosentizers

Over the last 30 years, sonodynamic therapy (SDT) has been under investigation as a treatment for malignant tumours. SDT utilizes ultrasound in combination with a sonosensitizer to cause cell death. While this treatment is in use, there remains critical questions that limit the translation of this promising therapy into the clinic. Chemical or physical changes occurring due to ultrasound may explain the efficacy observed and depending on the frequency and intensity of sound used, cavitation may be an important component of this. Some findings indicate that collapsing bubbles, or sonoluminescence, may cause the sonosensitizers to split, creating reactive oxygen species (ROS). Other research suggests damage to cell structure due to the ultrasound waves is the key. Understanding the required balance of chemical and physical effect for varied cancer cells is critical to optimization of the treatment. This paper presents a preliminary investigation of the cause of cell death observed in SDT, with focuses on ROS generation, the use of ultrasound to activate chemical compounds, and observable mechanical damage to cells following ultrasound exposure.