Keyse S M, Tyrrell R M
Swiss Institute for Experimental Cancer Research, Epalinges/Lausanne.
J Biol Chem. 1987 Oct 25;262(30):14821-5.
We have analyzed the pattern of protein synthesis in solar near ultraviolet (334 nm, 365 nm) and near visible (405 nm) irradiated normal human skin fibroblasts. Two hours after irradiation we find that one major stress protein of approximately 32 kDa is induced in irradiated cells. This protein is not induced by ultraviolet radiation at wavelengths shorter than 334 nm and is not inducible by heat shock treatment of these cells. Although sodium arsenite, diamide, and menadione all induced a 32-kDa protein, they also induced the major heat shock proteins. In contrast, the oxidizing agent, hydrogen peroxide, induced the low molecular weight stress protein without causing induction of the major heat shock proteins. A comparison of the 32-kDa proteins induced by sodium arsenite, H2O2, and solar near ultraviolet radiation using chemical peptide mapping shows that they are closely related. These results imply that the pathways for induction of the heat shock response and the 32-kDa protein are not identical and suggest that, at least in the case of radiation and treatment with H2O2, the 32-kDa protein might be induced in response to cellular oxidative stress. This conclusion is supported by the observation that depletion of endogenous cellular glutathione prior to solar near ultraviolet irradiation lowers the fluence threshold for induction of the 32-kDa stress protein.
我们分析了太阳能近紫外线（334nm、365nm）和近可见光（405nm）照射正常人类皮肤成纤维细胞后的蛋白质合成模式。照射两小时后，我们发现在照射细胞中诱导出一种约32kDa的主要应激蛋白。该蛋白在波长小于334nm的紫外线照射下不会被诱导，且对这些细胞进行热休克处理也不会诱导其产生。虽然亚砷酸钠、二酰胺和甲萘醌均能诱导出一种32kDa的蛋白，但它们也会诱导主要的热休克蛋白。相比之下，氧化剂过氧化氢能诱导低分子量应激蛋白，而不会诱导主要的热休克蛋白。使用化学肽图谱对亚砷酸钠、过氧化氢和太阳能近紫外线辐射诱导的3 kDa蛋白进行比较，结果表明它们密切相关。这些结果表明，热休克反应和32kDa蛋白的诱导途径并不相同，并表明至少在辐射和过氧化氢处理的情况下，32kDa蛋白可能是细胞氧化应激诱导产生的。内源性细胞谷胱甘肽在太阳能近紫外线照射前耗尽会降低诱导32kDa应激蛋白的通量阈值，这一观察结果支持了这一结论。
