Giordani A, Morlière P, Djavaheri-Mergny M, Santus R
Laboratoire de Photobiologie, INSERM U.312, Muséum National d'Histoire Naturelle, Paris, France.
Photochem Photobiol. 1998 Sep;68(3):309-13.
The aconitase activity of the cytoplasmic iron regulatory protein-1 of NCTC 2544 keratinocytes is effectively inhibited by physiological doses of UVA. The time course of the photoinactivation is biphasic. A fast step is first observed corresponding to about 50% inactivation after exposure to 5 J/cm2 of UVA followed by a much slower photoinactivation at higher doses. The water-soluble antioxidant N-acetylcysteine only partially inhibits the photoinduced inactivation of the cytoplasmic aconitase function, whereas the lipophilic vitamin E, the iron chelator, desferrioxamine and the superoxide dismutase inhibitor, diethyldithiocarbamate do not protect at all. As a consequence, reactive oxygen species such as O2-., H2O2 and lipid peroxides and hydroperoxides seem to play a rather minor role in the inactivation induced by the UVA photooxidative stress although an oxidative stress produced by O2-. and H2O2 is known to inhibit reversibly and effectively cytoplasmic aconitase activity in mammalian cells.
生理剂量的紫外线A(UVA)可有效抑制NCTC 2544角质形成细胞的细胞质铁调节蛋白-1的顺乌头酸酶活性。光失活的时间进程是双相的。首先观察到一个快速阶段,对应于暴露于5 J/cm²的UVA后约50%的失活,随后在更高剂量下光失活要慢得多。水溶性抗氧化剂N-乙酰半胱氨酸仅部分抑制细胞质顺乌头酸酶功能的光诱导失活,而亲脂性维生素E、铁螯合剂去铁胺和超氧化物歧化酶抑制剂二乙基二硫代氨基甲酸盐则完全没有保护作用。因此,尽管已知由超氧阴离子(O₂⁻·)和过氧化氢(H₂O₂)产生的氧化应激可在哺乳动物细胞中可逆且有效地抑制细胞质顺乌头酸酶活性,但活性氧如超氧阴离子(O₂⁻·)、过氧化氢(H₂O₂)以及脂质过氧化物和氢过氧化物在UVA光氧化应激诱导的失活中似乎起的作用较小。