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Rheumatology International

Erschienen in:

01.09.2003 | Original Article

Mechanisms of sodium nitroprusside-induced death in human chondrocytes

verfasst von: Klaus Kühn, Martin Lotz

Erschienen in: Rheumatology International | Ausgabe 5/2003

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Abstract

The nitric oxide (NO) donor sodium nitroprusside (SNP) has been used to study NO-dependent cell death in human chondrocytes. This study compares SNP-induced chondrocyte death and SNP-activated signaling mechanisms with apoptosis induced by CD95 activation. Sodium nitroprusside increased cell death dose-dependently. Compared to CD95 stimulation, SNP induced only low levels of internucleosomal DNA fragmentation as measured by cell-death enzyme-linked immunosorbent assay (ELISA). However, SNP caused substantial nuclear DNA cleavage, as evidenced by terminal deoxynucleotidyltransferase (TdT)-mediated deoxyuridine triphosphate (dUTP) nick end-labeling (TUNEL). Caspase-3 processing in response to SNP was not detected. The pancaspase inhibitor Z-VAD.FMK partially abrogated the TUNEL signal but did not block cell death or internucleosomal DNA fragmentation. The caspase-3-specific inhibitor Ac-DEVD-CHO did not inhibit the SNP-induced TUNEL signal or internucleosomal DNA fragmentation. DNA degradation was not blocked by the p38 inhibitor SB 202190 but by the reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine. The results of this study support the hypothesis that the phenotype and mechanisms of SNP-induced chondrocyte death are distinct from apoptosis induction via CD95.

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Titel: Mechanisms of sodium nitroprusside-induced death in human chondrocytes
verfasst von: Klaus Kühn
Martin Lotz
Publikationsdatum: 01.09.2003
Verlag: Springer-Verlag
Erschienen in: Rheumatology International / Ausgabe 5/2003
Print ISSN: 0172-8172
Elektronische ISSN: 1437-160X
DOI: https://doi.org/10.1007/s00296-003-0299-y

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