Chemo-sensitizing capability of DHA is mediated through generation of intracellular ROS and formation of lipid peroxides. Figure 5A illustrates mean relative fluorescence units ± SEM of MEC-2 over the course of 2 hours following 72 hour pre-treatment with vehicle, AA 25 μM, EPA 50 μM or DHA 50 μM. Linear regression analysis indicated a greater slope following treatment with EPA or DHA versus vehicle (0.483 and 0.683 versus 0.267) indicating an increased generation of ROS across time. Figure 5B illustrates mean ng MDA/μg protein ± SEM in the presence or absence of vehicle, AA 25 μM, EPA 50 μM or DHA 50 μM alone and following treatment with doxorubicin (1.5 μM) or vincristine (100 nM). Pre-treatment with DHA induced significantly higher levels of MDA as compared to vehicle. The addition of doxorubicin to DHA pre-treated cells induced significantly higher levels of MDA versus either alone. The addition of vincristine to either EPA or DHA pre-treated cells induced significantly lower levels of MDA as compared to n-3 or drug alone. Figure 5C illustrates the % cell viability ± SEM of MEC-2 following treatment with 1.5 μM doxorubicin and 50 μM vitamin-E alone and in combination in the presence or absence of vehicle, AA 25 μM, EPA 50 μM or DHA 50 μM. Compared to vehicle, cells pre-treated with DHA had significantly greater reductions in cell viability when treated with doxorubicin. Co-treatment of DHA pre-treated cells with doxorubicin and vitamin-E abrogated the enhanced sensitivity of MEC-2 to doxorubicin by DHA. Figure 5D illustrates mean ng MDA/μg protein ± SEM of MEC-2 following pre-treatment with DHA alone and after treatment with 1.5 μM doxorubicin alone and in combination with 50 μM vitamin-E. Co-treatment with doxorubicin and vitamin-E in DHA pre-treated cells indicated significantly lower levels of MDA versus doxorubicin alone. Statistical significance was determined by Multiple Comparison Test with Tukey’s correction. Abbreviations: MDA: malondialdehyde, α = 0.05, * <0.05, ** < 0.01, *** < 0.001.