Lipid peroxidation and oxidant stress regulate hepatic apolipoprotein B degradation and VLDL production
J. Clin. Invest. Meihui Pan, et al. 113:1277 doi:10.1172/JCI19197 [Go to this article.]

Figure 2
Cotreatment of McA cells with DHA and either an intracellular iron chelator or an antioxidant inhibits ApoB100 degradation and the increase in intracellular lipid peroxidation. (A) McA cells were pretreated for 1 hour with medium containing BSA or DHA/BSA complexes, followed by a 3-hour incubation in medium containing BSA, DHA/BSA, DHA/BSA plus 100 ∝M DFX, or DHA/BSA plus 120 ∝M vitamin E (vit E). Cells were then harvested for TBARS assays. *P < 0.01 vs. DHA. (B) McA cells were pretreated with BSA or DHA/BSA for 2 hours and then subjected to a pulse-chase study similar to that illustrated in Figure 1, except that DFX or vitamin E was administered 45 minutes before labeling and was present in the medium thereafter. The composite fluorogram displays representative total labeled ApoB100 recovery data, and the graph summarizes three complete experiments with each treatment applied to triplicate wells. *P < 0.01 vs. DHA. (C) A similar pulse-chase study was carried out, but DFX was replaced by the cell-impermeable iron chelator DTPA (100 ∝M). Recovery and fluorography of labeled ApoB100 were done as in Figure 1.