Polla B S, Kantengwa S, François D, Salvioli S, Franceschi C, Marsac C, Cossarizza A
Laboratoire de Physiologie Respiratoire, Unité de Formation et de Recherche Cochin Port-Royal, Paris, France.
Proc Natl Acad Sci U S A. 1996 Jun 25;93(13):6458-63. doi: 10.1073/pnas.93.13.6458.
Heat shock (HS) proteins (HSPs) induce protection against a number of stresses distinct from HS, including reactive oxygen species. In the human premonocytic line U937, we investigated in whole cells the effects of preexposure to HS and exposure to hydrogen peroxide (H2O2) on mitochondrial membrane potential, mass, and ultrastructure. HS prevented H2O2-induced alterations in mitochondrial membrane potential and cristae formation while increasing expression of HSPs and the protein product of bcl-2. Protection correlated best with the expression of the 70-kDa HSP, hsp70. We propose that mitochondria represent a selective target for HS-mediated protection against oxidative injury.
热休克（HS）蛋白（HSPs）可诱导对多种不同于热休克的应激产生保护作用，包括活性氧。在人早幼单核细胞系U937中，我们在全细胞水平研究了预先暴露于热休克以及暴露于过氧化氢（H₂O₂）对线粒体膜电位、质量和超微结构的影响。热休克可预防H₂O₂诱导的线粒体膜电位改变和嵴形成，同时增加HSPs和bcl-2蛋白产物的表达。保护作用与70 kDa HSP即hsp70的表达相关性最佳。我们提出，线粒体是热休克介导的抗氧化损伤保护作用的一个选择性靶点。
