Journal
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
Volume 437, Issue 1, Pages 96-105Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.abb.2005.02.023
Keywords
MnSOD; ATP; nitric oxide; oxidants; caspases; cytochrome c; apoptosis; Antimycin A; cells; nitrosylation
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Funding
- NIDDK NIH HHS [R01 DK59872-03] Funding Source: Medline
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We have previously shown that in vivo renal ischemia/reperfusion results in ATP depletion, oxidant production, and manganese superoxide dismutase (MnSOD) inactivation. Current Studies were designed to compare the effect of ATP depletion (Antimycin A treatment) on cell death pathways using renal proximal tubular cells and identical cells that overexpress MnSOD. ATP depletion in wild-type cells induced an apoptotic cascade that involved caspase 9 activation; MnSOD overexpressing cells afforded protection against apoptosis. This protection did not appear to involve a cytochrome e-related mechanism, but may be related to altered levels of nitric oxide within the cell. Further studies suggested that nitric oxide was required to protect the renal cells from caspase-rnediated cell death. Interestingly, treatment of renal cell extracts with reductants (DTT and ascorbate) enhanced caspase activation. Taken together, these results suggest that cysteine nitrosylation may be playing a role in caspase dysfunction in cells overexpressing MnSOD following ATP depletion. (c) 2005 Elsevier Inc. All rights reserved.
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