Lipid photooxidation in erythrocyte ghosts: Sensitization of the membranes toward ascorbate- and superoxide-induced peroxidation and lysis

摘要: The damaging effects of ascorbate (AH−) and superoxide (O2−) on resealed erythrocyte ghosts containing predetermined levels lipid hydroperoxides (LOOHs) have been studied. Continuous blue light irradiation membranes in the presence protoprophyrin resulted steadily increasing LOOH enhanced release a trapped marker, glucose 6-phosphate (G6P), after 3- to 4-h lag. Neither dismutase (SOD) nor catalase inhibited these effects, ruling out O2− H2O2 as reactive intermediates. A 1-h dose produced partially photoperoxidized ghosts, which, dark at 37 °C, released G6P no faster than unirradiated controls (~7%/h). When xanthine oxidase plus (XO/X) was introduced source H2O2, irradiated lysed rapidly (t12 ~ 2 h). EDTA or SOD reaction, whereas had little effect. Unirradiated were not by XO/X unless system supplemented with Fe(III), which case total protection afforded catalase. In all experiments there an excellent correlation between postirradiation peroxidation (thiobarbituric acid reactivity) release. Similar observations made AH−. For example, incubation photooxidized 0.5 mm AH− rapid lysis 1 h), stimulated twofold 50 μm Fe(III) EDTA. By comparison, showed net 3 h exposure Fe(III)/AH−. protected against AH−-stimulated damage. -promoted butylated hydroxytoluene, lipophilic antioxidant, but unaffected 2,5-dimethylfuran ethanol, singlet oxygen, hydroxyl radical traps, respectively. These results suggest that mechanism exists photogenerated LOOHs undergo redox metalmediated reduction alkoxy radicals (LO•), trigger burst membrane-disrupting peroxidation.