Gaboriau F, Morlière P, Marquis I, Moysan A, Gèze M, Dubertret L
Laboratoire de Physique et Chimie Biomoléculaires, CNRS U.A. 198, Institut Curie, Paris, France.
Photochem Photobiol. 1993 Oct;58(4):515-20. doi: 10.1111/j.1751-1097.1993.tb04924.x.
Irradiation of cultured human skin fibroblasts with ultraviolet light from 320 to 400 nm (UVA) leads to a decrease in the membrane fluidity exemplified by an enhanced fluorescence anisotropy of the lipophilic fluorescent probe 1-[4-trimethylamino)-phenyl]-6-phenylhexa-1,3,5-triene. This UVA-induced decrease in fluidity is associated with lactate dehydrogenase leakage in the supernatant. Vitamin E, an inhibitor of lipid peroxidation, exerts a protective effect on both phenomena. Therefore, this UVA-induced damage in membrane properties may be related to lipid peroxidation processes. Moreover, exponentially growing cells are more sensitive to these UVA-induced alterations than confluent cells.
用320至400纳米的紫外线(UVA)照射培养的人皮肤成纤维细胞,会导致膜流动性降低,这表现为亲脂性荧光探针1-[4-(三甲氨基)苯基]-6-苯基-1,3,5-己三烯的荧光各向异性增强。这种UVA诱导的流动性降低与上清液中乳酸脱氢酶的泄漏有关。维生素E是一种脂质过氧化抑制剂,对这两种现象都有保护作用。因此,这种UVA诱导的膜特性损伤可能与脂质过氧化过程有关。此外,指数生长期的细胞比汇合细胞对这些UVA诱导的变化更敏感。