Abstract Sonoporation is a developing technique used in drug delivery for cancer cells. Low frequency ultrasound is used to trigger the cavitation of microbubbles to puncture the cell membrane, and during this process, lipid metabolism becomes disrupted. In this study, cell viability and the generation of specific oxidized lipid products were assessed in Jurkat cells before and after sonoporation. A reduction in cell viability and an induction of apoptosis of Jurkat cells were found 4h and 24h post-sonoporation, respectively. Sonoporation suppressed cholesterol concentration and arachidonic, eicosapentaenoic and docosahexaenoic acids in the Jurkat cells. Levels of enzyme-independent oxidized products (F2-isoprostanes, F3-isoprostanes, 7-ketocholesterol) were elevated by sonoporation compared with the control, whereas enzyme-dependent oxidized products (5(S)-, 9(S)-, 12(S)-, 15(S)- and 20-HETE and 27-hydroxycholesterol) were not altered. Antioxidant enzymes activities were also increased in sonoporated Jurkat cells compared with the control. In this study, the loss of lipids potentially increased the availability for enzyme-independent lipid peroxidation, leading to cell fragility and death.