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Am J Physiol Cell Physiol 279: C452-C460, 2000;
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Vol. 279, Issue 2, C452-C460, August 2000

Contrasting effects of NO and peroxynitrites on HSP70 expression and apoptosis in human monocytes

Christophe Adrie1,2, Christoph Richter3, Maria Bachelet1, Nathalie Banzet1, Dominique François1, A. Tuan Dinh-Xuan1, Jean François Dhainaut2, Barbara S. Polla1, and Marie-Jeanne Richard1,4

1 Laboratory of Respiratory Physiology, Unité de Formation et de Recherche Cochin Port-Royal, Paris V University, and 2 Medical Intensive Care Unit, Cochin Port-Royal Hospital, Paris, France; 3 Institute of Biochemistry, Swiss Federal Institute of Technology, Zurich, Switzerland; and 4 Laboratory of Biology of Oxidative Stress, Biochemistry C, A. Michallon Hospital, Grenoble, France

The free radicals nitric oxide (·NO) and superoxide (O2-·) react to form peroxynitrite (ONOO-), a highly toxic oxidant species. In this study we investigated the respective effects of NO and ONOO- in monocytes from healthy human donors. Purified monocytes were incubated for 6 or 16 h with a pure NO donor (S-nitroso-N-acetyl-DL-penicillamine, 0-2 mM), an ·NO/ONOO- donor (3-morpholinosydnonimine chlorhydrate, 0-2 mM) with and without superoxide dismutase (200 IU/ml), or pure ONOO-. We provide evidence that 3-morpholinosydnonimine chlorhydrate alone represents a strong stress to human monocytes leading to a dose-dependent increase in heat shock protein-70 (HSP70) expression, mitochondrial membrane depolarization, and cell death by apoptosis and necrosis. These phenomena were abolished by superoxide dismutase, suggesting that ONOO-, but not ·NO, was responsible for the observed effects. This observation was further strengthened by the absence of a stress response in cells exposed to S-nitroso-N-acetyl-DL-penicillamine. Conversely, exposure of cells to ONOO- alone also induced mitochondrial membrane depolarization and cell death by apoptosis and necrosis. Thus ONOO- formation may well explain the toxic effect generally attributed to ·NO.

nitric oxide; heat shock; cell stress; cell death


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