In plants many biotic and abiotic stresses can cause secondary oxidative stress. Earlier work showed that, depending on the severity of the oxidative stress, plants can activate either cell protective genes or programmed cell death (PCD). Poly(ADP-ribose) polymerase (PARP) has been implicated as one of the enzymes in the apoptotic pathways induced by DNA damaging agents or oxidative stress. We show that in cultured soybean cells, PARP is involved in responses to mild and severe oxidative stresses, by mediating DNA repair and PCD processes, respectively. Addition of PARP inhibitors reduced the degree of cell death triggered by H2O2. Two windows of NAD consumption after H2O2 treatment were detected. Experiments with transient overexpression of Arabidopsis PARP cDNA promoted DNA repair and inhibited cell death caused by mild oxidative stress. However, following severe stress PARP overexpression increased cell death. Expression of antisense PARP produced the opposite effects: an increase in DNA nicks and inhibition of cell death at high, but not mild doses of H2O2. Copyright (C) 1998 Federation of European Biochemical Societies.
Bibliographical noteFunding Information:
We thank M. Chevion from the Hadassah Medical School, Jerusalem for performing the 8-hydroxy-2-deoxyguanosine measurements. This research was supported by a grant from the Binational (US-Israel) Science Foundation.
- Nicotinamide adenine dinucleotide
- Oxidative stress
- Poly(ADP-ribose) polymerase
- Programmed cell death