{'fraction_non_alphanumeric': 0.04468864468864469, 'fraction_numerical': 0.017582417582417582, 'mean_word_length': 5.898989898989899, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Reduction of a Nitroxide Spin Label by Native and Partially Oxidized Human Low‐Density Lipoprotein

The reduction of nitroxide compounds in vivo has in most part been assigned to the reaction with reductants such as ascorbic acid, reduced thiols and quinols such as ubiquinol or by reaction with simple carbon‐centred radicals. In this study a water‐soluble nitroxide, 2,2,5,5‐tetramethyl‐4‐phenylimidazolin‐3‐oxide‐1‐oxyl (TPI), was exposed to both native and partially oxidized human low‐density lipoprotein (LDLn and LDLpox, respectively) and it was found that TPI decayed in each case to the corresponding hydroxylamine, 2,2,5,5‐tetramethyl‐4‐phenyl‐3‐oxide‐1‐hydroxylimidazoline (TPHI). In particular, the reduction of TPI in the presence of LDLpox occurred via a complex mechanism involving the consumption of both α‐tocopherol (α‐TOH) and cholesteryl linoleate hydroperoxides (Ch18:2‐OOH). The EPR signal of the nitroxide also diminished when TPI was exposed to the water‐soluble vitamin E analogue, Trolox C, but neither Ch18:2‐OOH nor linoleate hydroperoxides alone caused significant decay of the nitroxide signal. Together these results indicate that water‐soluble nitroxides may be reduced in circulation by reaction with α‐TOH in LDL, thereby adding to the complexity of the reduction of nitroxide spin labels in vivo. © 1997 by John Wiley & Sons, Ltd.