Past studies investigating the regulatory functions of nitric oxide (NO) in plant cells have utilized various NO-donors that release NO in different redox forms, which has lead to problems in the interpretation of data. In the present study, the effects of different NO-donors releasing NO with either NO+ (SNP) or NO' (SNAP, GSNO, NOC-18) character have been compared in plant cells. In particular, ferritin regulation, programmed cell death, cellular redox state, and ROS-scavenging enzymes in Arabidopsis thaliana and Nicotiana tabacum cells were examined. The results show that SNP behaves differently than the other NO-donors tested; indeed, SNP induces accumulation of ferritin transcripts in Arabidopsis, whereas SNAP inhibits its accumulation. Moreover, among the assortment of donors tested, only SNP caused programmed cell death and suppression of ROS-scavenging systems.

Comparative effects of various nitric oxide donors on ferritin regulation, programmed cell death and cell redox state in plant cells.

2004

Abstract

Past studies investigating the regulatory functions of nitric oxide (NO) in plant cells have utilized various NO-donors that release NO in different redox forms, which has lead to problems in the interpretation of data. In the present study, the effects of different NO-donors releasing NO with either NO+ (SNP) or NO' (SNAP, GSNO, NOC-18) character have been compared in plant cells. In particular, ferritin regulation, programmed cell death, cellular redox state, and ROS-scavenging enzymes in Arabidopsis thaliana and Nicotiana tabacum cells were examined. The results show that SNP behaves differently than the other NO-donors tested; indeed, SNP induces accumulation of ferritin transcripts in Arabidopsis, whereas SNAP inhibits its accumulation. Moreover, among the assortment of donors tested, only SNP caused programmed cell death and suppression of ROS-scavenging systems.
2004
Istituto di Biofisica - IBF
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.14243/162393
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