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Rotenone and pyruvate prevent the tert ‐butylhydroperoxide‐induced necrosis of U937 cells and allow them to proliferate
Author(s) -
Sestili Piero,
Brambilla Liliana,
Cantoni Orazio
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)01027-3
Subject(s) - rotenone , mitochondrial permeability transition pore , mitochondrion , microbiology and biotechnology , u937 cell , membrane permeability , inner mitochondrial membrane , necrosis , tumor necrosis factor alpha , programmed cell death , chemistry , biology , biochemistry , apoptosis , membrane , immunology , genetics
Exposure of U937 cells to tert ‐butylhydroperoxide (tB‐OOH) led to cyclosporin A‐sensitive mitochondrial membrane permeability transition and necrosis. Pyruvate and rotenone, which increase mitochondrial NADH via different mechanisms, prevented these responses and the cells which received these treatments proliferated with kinetics similar to those observed in untreated cells. In contrast with these results, cells rescued by cyclosporin A were unable to proliferate. Thus, mitochondrial NADH plays a pivotal role in preventing upstream events which result in the onset of mitochondrial membrane permeability transition and death in cells exposed to tB‐OOH. These events appear to be critical for recovery of the ability of the cells to proliferate.