标题：Suppressive Effects of Flavonoids and α-Tocopherol on the Linoleic Acid Hydroperoxide-induced Generation of Reactive Oxygen Species in Rat Pheochromocytoma PC12 Cells
期刊名称：Journal of Clinical Biochemistry and Nutrition
印刷版ISSN：0912-0009
电子版ISSN：1880-5086
出版年度：2003
卷号：33
期号：1
页码：13-22
DOI：10.3164/jcbn.33.13
出版社：The Society for Free Radical Research Japan
摘要：It was found using the fluorescence probe 2′, 7′-dichlorofluorescin diacetate that linoleic acid hydroperoxide (LOOH) increased the level of reactive oxygen species in rat pheochromocytoma PC12 cells in a dose-dependent manner. Eight flavonoids, including apigenin, eriodictyol, 3-hydroxyflavone, kaempherol, luteolin, naringenin, quercetin, and taxifolin, and α-tocopherol, suppressed the LOOH-induced increase in the intracellular level of reactive oxygen species; α-tocopherol was used as a positive control. On coincubation of cells with each flavonoid and LOOH, the suppressive efficacy of the flavonoids against the LOOH-induced increase was in the following order: luteolin≥3-hydroxyflavone>kaempherol≈quercetin>eriodictyol>taxifolin>apigenin>>naringenin. Luteolin and 3-hydroxyflavone were more effective than α-tocopherol. Kaempherol and quercetin were as similarly effective as it. On preincubation of cells with each flavonoid prior to LOOH exposure, the suppressive efficacy of the flavonoids against the LOOH-induced increase was in the following order: luteolin≈quercetin<3-hydroxyflavone>taxifolin>eriodictyol>naringenin>kaempherol>apigenin. Luteolin, quercetin, and 3-hydroxyflavone were as similarly effective as α-tocopherol. Further, the iron ion chelating agents desferrioxamine mesylate and disodium bathophenanthrolinedisulfonate suppressed the LOOH-induced increase. Reactive oxygen species such as the hydroxyl and alkoxyl radicals may be generated from LOOH in the presence of iron ions in cells and may be scavenged by the flavonoids. These results suggest that such flavonoids as luteolin, 3-hydroxyflavone, and quercetin are beneficial for neuronal cells under reactive oxygen species-induced oxidative stress.
