期刊
JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
卷 129, 期 19, 页码 6088-+出版社
AMER CHEMICAL SOC
DOI: 10.1021/ja0689785
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资金
- NEI NIH HHS [R01 EY016813, EY016813] Funding Source: Medline
- NHLBI NIH HHS [HL53315, R01 HL053315] Funding Source: Medline
- NIGMS NIH HHS [R01 GM021249, GM21249] Funding Source: Medline
The formation of cytotoxic gamma-hydroxyalkenals has been generally viewed as the consequence of free radical-induced oxidation of polyunsaturated fatty acyls through the decomposition of lipid peroxides. Vitamin E (Vit E) would be expected to inhibit such autoxidation. In a model study, we now find that fragmentation of a hydroperoxy endoperoxide generated the lactone of a gamma-hydroxyalkenal. With 1 equiv of Fe2+, or with a catalytic amount (0.1 equiv) of Fe2+ and 1 equiv of Vit E, the yields are 43-50%. However, Vit E alone did not promote the fragmentation, and a catalytic amount of Fe2+ alone only afforded a low yield (about 5%). Vit E could contribute to, as opposed to preventing, the formation of gamma-hydroxyalkenals by converting redox-active metal ions into their reduced forms that promote the rapid fragmentation of hydroperoxy endoperoxides.
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