Bose B, Chatterjee S N
Biophysics Division, Saha Institute of Nuclear Physics, Calcutta, India.
J Photochem Photobiol B. 1994 May;23(2-3):119-23. doi: 10.1016/1011-1344(94)06995-6.
Exposure of a dried lipid thin film to UVA produced a dose-dependent linear increase in the three peroxidation products, conjugated diene, lipid hydroperoxide and malondialdehyde (MDA). All three lipid peroxidation products exhibited an inverse dose rate effect. Identical amounts of malondialdehyde were produced when the lipid film was exposed to UVA either directly or through the thickness of the Corning glass on which the film was cast. Antioxidants, alpha-tocopherol, butylated hydroxytoluene (BHT) and the singlet oxygen quencher beta-carotene significantly inhibited the UVA-induced peroxidation of the lipid film. The biological implications of the UVA-induced peroxidation of the dried lipid film are discussed.
将干燥的脂质薄膜暴露于UVA下,会使三种过氧化产物(共轭二烯、脂质氢过氧化物和丙二醛(MDA))呈现出剂量依赖性线性增加。所有这三种脂质过氧化产物均表现出反剂量率效应。当脂质薄膜直接暴露于UVA或通过其所在的康宁玻璃厚度暴露于UVA时,会产生相同量的丙二醛。抗氧化剂α-生育酚、丁基化羟基甲苯(BHT)和单线态氧猝灭剂β-胡萝卜素可显著抑制UVA诱导的脂质薄膜过氧化。本文讨论了UVA诱导干燥脂质薄膜过氧化的生物学意义。