The present study was initiated to investigate the potential
biological mechanism of cell killing effect on isolate
sarcoma 180 (S180) cells induced by ultrasound activating
protoporphyrin IX (
PPIX). S180 cells were exposed to ultrasound for 30s duration, at a frequency of 2.2 MHz and an acoustic power of 3 W/cm(2) in the presence of 120 microM
PPIX. The viability of cells was evaluated using
trypan blue staining. The generation of
oxygen free radicals in cell
suspensions was detected immediately
after treatment using a reactive
oxygen detection kit. A
copper reagent colorimetry method was used to measure the level of FFAs released into cell
suspensions by the process of cell damage induced by ultrasound and
PPIX treatment. Oxidative stress was assessed by measuring the activities of key
antioxidant enzymes (i.e., SOD, CAT, GSH-PX) in S180
tumor cells. Treatment with ultrasound and
PPIX together increased the cell damage rate to 50.91%, while treatment with ultrasound alone gave a cell damage rate to 24.24%, and
PPIX alone kept this rate unchanged. Colorimetry and enzymatic chemical methods showed that the level of FFAs in cell
suspension increased significantly after the treatment, while the activity of all the above
enzymes decreased in
tumor cells at different levels, and were associated with the generation of
oxygen free radicals in cell
suspension after treatment. The results indicate that
oxygen free radicals may play an important role in improving the
membrane lipid peroxidation, degrading membrane
phospholipids to release FFAs, and decreasing the activities of the key
antioxidant enzymes in cells. This
biological mechanism might be involved in mediating the effects on S180 cells and resulting in the cell damage seen with SDT.