UVB Induced Photooxidation of Vitamin E

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Abstract
The photochemistry of α-tocopherol (α-TH, vitamin E) may contribute to its inhibition of UVB (290−320 nm) photocarcinogenesis. Photochemical reactions of α-TH were studied by monitoring the fate of α-TH in UVB irradiated liposomes and solution. Soy phosphatidylcholine (SPC) and dioleoylphosphatidylcholine (DOPC) liposomes were supplemented with α-TH (1.0 mol % α-TH/phospholipid) and irradiated with UVB at a dose rate of 6.0 J m-2 s-1 for up to 90 min. α-TH was rapidly depleted in UVB irradiated liposomes. Oxidative damage, assessed by monitoring lipid peroxidation, was suppressed in SPC liposomes until α-TH was depleted to 20% of initial levels. α-TH also was rapidly depleted by UVB irradiation in acetonitrile/H2O (4:1 v/v) solution. In SPC liposomes, products previously identified as marker products for peroxyl radical scavenging by α-TH were observed, including α-tocopherol quinone, 5,6-epoxy-α-tocopherol quinone, and 2,3-epoxy-α-tocopherol quinone. These products also were formed in DOPC liposomes, which are resistant to lipid peroxyl radical formation. In addition, an α-tocopherol dihydroxy dimer and several 8a-(hydroperoxy)epoxytocopherones were identified by HPLC and HPLC-MS. The dimer appears to result from recombination of photoinduced tocopheroxyl radicals. Products associated with peroxyl radical scavenging (quinones, epoxyquinones, 8a-(hydroperoxy)epoxytocopherones) and with UVB dependent production of tocopheroxyl radicals (dihydroxy dimer) also were found when α-TH was oxidized by UVB in acetonitrile. Because the acetonitrile contained no autoxidizable substrate, formation of peroxyl radical derived products may occur via intermediate tocopherone peroxyl radicals. These results indicate that α-TH photooxidation proceeds via competing reactions of UVB induced tocopheroxyl radicals.