Skip to main content

Alteration in ascorbate and ascorbate peroxidase in programmed cell death and oxidative stress

Different stress conditions, of biotic and abiotic nature, enhance the cellular production of reactive oxygen species (ROS) [1]. Due to their reactive nature, ROS are potentially harmful to all cellular components. Apart their destructive nature, ROS behave as metabolic regulators, being considered as secondary messengers. Indeed, ROS can trigger pathways aimed at saving cells from demise; however, under certain conditions, they can also impair the cellular red/ox balance as to activate a programmed cell death (PCD) process [2, 3]. These differences in the ROS-dependent responses seem to be due to different localization, timing and level of ROS production under different stimuli [4, 5]. Moreover, the possibility that the co-production of other reactive species is a critical point for the activation of different defence responses has been recently underlined. Increasing attention has been paid to nitric oxide (NO) as a signal molecule synergically acting with ROS in the activation of PCD [6, 7]. The level of ROS and the cellular redox homeostasis are regulated by different antioxidant systems; among these, ascorbate (ASC) plays a pivotal role, it being both a direct scavenger of ROS and the electron donor of ascorbate peroxidase (APX), a key enzyme for scavenging hydrogen peroxide in plant cells [8, 9].

Here we report data showing that in tobacco cultured cells a moderate oxidative stress did not lead to apoptotic or necrotic events whereas, when H2O2 production was increased over a certain range of concentration, an induction of cell death with the features of necrosis was achieved. On the other hand, when the tobacco cells were simultaneous treated with NO and H2O2 generators a PCD program was triggered. The scavengers ASC and APX change differently under the various stress conditions. During the moderate oxidative stress a transient increase in APX activity occurred whereas, in the induction of cell necrosis, the activity of APX decreased proportionally to cell death. Under such conditions, no alteration in the APX gene expression was evident and 24 hours after the generation of the oxidative stress, APX activity was significantly increased in the surviving cells, in order to overcome the oxidative stress and to avoid further cell death. When the PCD program was triggered in these cells by the contemporary increase of NO and H2O2 the suppression of APX occurred both at the translation or post-translation level. The decrease in APX seems to be one of the first alteration in the redox regulating systems induced in the plant cells in route to PCD.


  1. Dat J, Vandenabeele S, Vranovà E, Van Montagu M, Inzè D, Van Breusegem F: Dual action of the active oxygen species during plant stress responses. Cell Mol Life Sci. 2000, 57: 779-795. 10.1007/s000180050041.

    Article  CAS  PubMed  Google Scholar 

  2. Lam E, Kato N, Lawton M: Programmed cell death, mitochondria and the plant hypersensitive response. Nature. 2001, 411: 848-853. 10.1038/35081184.

    Article  CAS  PubMed  Google Scholar 

  3. Vacca RA, de Pinto MC, Valenti D, Passarella S, Marra E, De Gara L: Production of reactive oxygen species, alteration of cytosolic ascorbate peroxidase and impairment of mitochondria metabolism are early events in heat shock-induced programmed cell death in tobacco bright-Yellow 2 cells. Plant Physiol. 2004, 134: 1100-1112. 10.1104/pp.103.035956.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  4. Mittler R: Oxidative stress, antioxidants and stress tolerance. Trends Plant Sci. 2002, 7: 405-410. 10.1016/S1360-1385(02)02312-9.

    Article  CAS  PubMed  Google Scholar 

  5. De Gara L, de Pinto MC, Tommasi F: The antioxidant systems vis à vis reactive oxygen species during plant-pathogen interaction. Plant Physiol Biochem. 2003, 41: 863-870. 10.1016/S0981-9428(03)00135-9.

    Article  CAS  Google Scholar 

  6. Delledonne M, Xia Y, Dixon RA, Lamb C: Nitric oxide functions as a signal in plant disease resistance. Nature. 1998, 394: 585-588. 10.1038/29087.

    Article  CAS  PubMed  Google Scholar 

  7. de Pinto MC, Tommasi F, De Gara L: Changes in the antioxidant systems as part of the signaling pathway responsible for the programmed cell death activated by nitric oxide and reactive oxygen species in tobacco Bright-Yellow 2 cells. Plant Physiol. 2002, 130: 698-708. 10.1104/pp.005629.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  8. Smirnoff N: Ascorbic acid: metabolism and functions of a multi-facetted molecule. Curr Opin Plant Biol. 2000, 3: 229-235.

    Article  CAS  PubMed  Google Scholar 

  9. Noctor G, Foyer CH: Ascorbate and glutathione: keeping active oxygen under control. Annu Rev Plant Physiol Plant Mol Biol. 1998, 49: 249-279. 10.1146/annurev.arplant.49.1.249.

    Article  CAS  PubMed  Google Scholar 

Download references

Author information

Authors and Affiliations


Corresponding author

Correspondence to Maria Concetta de Pinto.

Rights and permissions

Open Access This article is published under license to BioMed Central Ltd. This is an Open Access article is distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Reprints and permissions

About this article

Cite this article

Paradiso, A., Tommasi, F., De Gara, L. et al. Alteration in ascorbate and ascorbate peroxidase in programmed cell death and oxidative stress. BMC Plant Biol 5 (Suppl 1), S28 (2005).

Download citation

  • Published:

  • DOI: