Klotz L O, Pellieux C, Briviba K, Pierlot C, Aubry J M, Sies H
Institut für Physiologische Chemie I, Heinrich-Heine-Universität Düsseldorf, Germany.
Eur J Biochem. 1999 Mar;260(3):917-22. doi: 10.1046/j.1432-1327.1999.00255.x.
Ultraviolet A (UVA; 320-400 nm) radiation in human skin fibroblasts induces a pattern of mitogen-activated protein kinase (MAPK) activation consisting of a rapid and transient induction of p38 and c-Jun-N-terminal kinase (JNK) activity but not extracellular signal-regulated kinases (ERK). UVA activation of p38 can be inhibited by the singlet oxygen (1O2) quenchers azide and imidazole, but not by the hydroxyl radical scavengers mannitol or dimethylsulfoxide, pointing to the involvement of 1O2. The same effect has been shown for JNK. Like UVA, 1O2 generated intracellularly upon photoexcitation of Rose Bengal activates p38 and JNK but not ERK. p38 and JNK activation was also elicited by chemiexcitation for the intracellular generation of 1O2 by the lipophilic 1,4-endoperoxide of N,N'-di(2,3-dihydroxypropyl)-1, 4-naphthalene dipropionamide. In contrast, extracellular generation of 1O2, by irradiation of Rose Bengal immobilized on agarose beads or by chemiexcitation employing the hydrophilic 1,4-endoperoxide of disodium 3,3'-(1,4-naphthylidene) dipropionate, was ineffective in activating p38 or JNK. These data suggest that the activation of p38 and JNK by 1O2 occurs only when the electronically excited molecule is generated intracellularly.
紫外线A（UVA；320 - 400纳米）辐射可在人皮肤成纤维细胞中诱导丝裂原活化蛋白激酶（MAPK）的激活模式，包括快速且短暂地诱导p38和c-Jun氨基末端激酶（JNK）的活性，但不诱导细胞外信号调节激酶（ERK）的活性。p38的UVA激活可被单线态氧（1O2）淬灭剂叠氮化物和咪唑抑制，但不能被羟基自由基清除剂甘露醇或二甲基亚砜抑制，这表明1O2参与其中。JNK也有同样的效应。与UVA一样，孟加拉玫瑰红光激发后在细胞内产生的1O2可激活p38和JNK，但不激活ERK。通过亲脂性的N，N'-二（2，3 - 二羟基丙基）-1，4 - 萘二丙酰胺的1，4 - 内过氧化物进行化学激发以在细胞内产生1O2，也能引发p38和JNK的激活。相反，通过照射固定在琼脂糖珠上的孟加拉玫瑰红或使用亲水性的3，3'-（1，4 - 萘亚基）二丙酸钠的1，4 - 内过氧化物进行化学激发在细胞外产生1O2，对激活p38或JNK无效。这些数据表明，只有当电子激发分子在细胞内产生时，1O2才能激活p38和JNK。
