Dissociation of atherogenesis from aortic accumulation of lipid hydro(pero)xides in Watanabe heritable hyperlipidemic rabbits
J. Clin. Invest. Paul Witting, et al. 104:213 doi:10.1172/JCI6391 [Go to this article.]

Figure 1
LDL from WHHL rabbits treated with probucol or bisphenol is resistant to ex vivo lipid peroxidation induced by AAPH. Pooled LDL (0.5-0.6 mg protein/mL) from rabbits fed probucol (filled circles), bisphenol (filled squares), control diets (filled triangles), or control LDL + BHT (10 μM) (filled diamonds) was treated at 37°C with 2 mM AAPH. Aliquots were removed and analyzed for α-TOH (a) and LO(O)H (b). LDL from bisphenol-treated (c) and probucol-treated (d) rabbits was also analyzed for bisphenol (open squares), diphenoquinone (open circles), and probucol (cross-hatched squares). Data represent mean ± SD of 4 independent studies. Initial concentrations (i.e., 100%) of α-TOH were 13 ± 2, 13 ± 3, 15 ± 2, and 15 ± 6 for probucol-treated, bisphenol-treated, control, and BHT-treated LDL, respectively. Initial levels of bisphenol and diphenoquinone were 10 ± 2 and 8 ± 1 μM and 12 ± 2 and 10 ± 3 μM for LDL from bisphenol- and probucol-treated rabbits, respectively. Initial levels of diphenoquinone were 1.6 ± 0.7 and 1.0 ± 0.1 μM for bisphenol and probucol samples, respectively. Probucol was expressed as percent peak area relative to that before oxidation. BHT-free control LDL oxidized to LO(O)H in a chain reaction, with chain length υ∼15 (see ref. 16 for determination of υ).