UVB Induced Photooxidation of Vitamin E
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- 作者：Kimberly A. Kramer and Daniel C. Liebler
- 刊名：Chemical Research in Toxicology
- 出版年：1997
- 出版时间：February 1997
- 年：1997
- 卷：10
- 期：2
- 页码：219 - 224
- 全文大小：187K
- 年卷期：v.10,no.2(February 1997)
- ISSN：1520-5010
文摘
The photochemistry of 
-tocopherol (-TH, vitamin E) maycontribute to its inhibition ofUVB (290-320 nm) photocarcinogenesis. Photochemical reactions of-TH were studied bymonitoring the fate of -TH in UVB irradiated liposomes and solution.Soy phosphatidylcholine(SPC) and dioleoylphosphatidylcholine (DOPC) liposomes weresupplemented with -TH (1.0mol % -TH/phospholipid) and irradiated with UVB at a dose rate of6.0 J m-2 s-1 forup to 90min. -TH was rapidly depleted in UVB irradiated liposomes.Oxidative damage, assessedby monitoring lipid peroxidation, was suppressed in SPC liposomes until-TH was depletedto 20% of initial levels. -TH also was rapidly depleted by UVBirradiation in acetonitrile/H2O (4:1 v/v) solution. In SPC liposomes, productspreviously identified as marker productsfor peroxyl radical scavenging by -TH were observed, including-tocopherol quinone, 5,6-epoxy--tocopherol quinone, and 2,3-epoxy--tocopherol quinone.These products also wereformed in DOPC liposomes, which are resistant to lipid peroxyl radicalformation. In addition,an -tocopherol dihydroxy dimer and several8a-(hydroperoxy)epoxytocopherones were identified by HPLC and HPLC-MS. The dimer appears to result fromrecombination of photoinducedtocopheroxyl radicals. Products associated with peroxyl radicalscavenging (quinones, epoxyquinones, 8a-(hydroperoxy)epoxytocopherones) and with UVBdependent production oftocopheroxyl radicals (dihydroxy dimer) also were found when -TH wasoxidized by UVB inacetonitrile. Because the acetonitrile contained no autoxidizablesubstrate, formation of peroxylradical derived products may occur via intermediate tocopherone peroxylradicals. These resultsindicate that -TH photooxidation proceeds via competing reactions ofUVB induced tocopheroxyl radicals.
-tocopherol (-TH, vitamin E) maycontribute to its inhibition ofUVB (290-320 nm) photocarcinogenesis. Photochemical reactions of-TH were studied bymonitoring the fate of -TH in UVB irradiated liposomes and solution.Soy phosphatidylcholine(SPC) and dioleoylphosphatidylcholine (DOPC) liposomes weresupplemented with -TH (1.0mol % -TH/phospholipid) and irradiated with UVB at a dose rate of6.0 J m-2 s-1 forup to 90min. -TH was rapidly depleted in UVB irradiated liposomes.Oxidative damage, assessedby monitoring lipid peroxidation, was suppressed in SPC liposomes until-TH was depletedto 20% of initial levels. -TH also was rapidly depleted by UVBirradiation in acetonitrile/H2O (4:1 v/v) solution. In SPC liposomes, productspreviously identified as marker productsfor peroxyl radical scavenging by -TH were observed, including-tocopherol quinone, 5,6-epoxy--tocopherol quinone, and 2,3-epoxy--tocopherol quinone.These products also wereformed in DOPC liposomes, which are resistant to lipid peroxyl radicalformation. In addition,an -tocopherol dihydroxy dimer and several8a-(hydroperoxy)epoxytocopherones were identified by HPLC and HPLC-MS. The dimer appears to result fromrecombination of photoinducedtocopheroxyl radicals. Products associated with peroxyl radicalscavenging (quinones, epoxyquinones, 8a-(hydroperoxy)epoxytocopherones) and with UVBdependent production oftocopheroxyl radicals (dihydroxy dimer) also were found when -TH wasoxidized by UVB inacetonitrile. Because the acetonitrile contained no autoxidizablesubstrate, formation of peroxylradical derived products may occur via intermediate tocopherone peroxylradicals. These resultsindicate that -TH photooxidation proceeds via competing reactions ofUVB induced tocopheroxyl radicals.