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Production of reactive species and modulation of antioxidant network in response to heat shock: a critical balance for cell fate
Author(s) -
LOCATO VITTORIA,
GADALETA COSIMO,
DE GARA LAURA,
DE PINTO MARIA CONCETTA
Publication year - 2008
Publication title -
plant, cell and environment
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.646
H-Index - 200
eISSN - 1365-3040
pISSN - 0140-7791
DOI - 10.1111/j.1365-3040.2008.01867.x
Subject(s) - apx , reactive oxygen species , catalase , oxidative stress , glutathione , antioxidant , microbiology and biotechnology , chemistry , programmed cell death , peroxidase , enzyme , biochemistry , homeostasis , heat shock protein , glutathione peroxidase , biology , apoptosis , gene
Exposure to adverse temperature conditions is a common stress factor for plants. In order to cope with heat stress, plants activate several defence mechanisms responsible for the control of reactive oxygen species (ROS) and redox homeostasis. Specific heat shocks (HSs) are also able to activate programmed cell death (PCD). In this paper, the alteration of several oxidative markers and ROS scavenging enzymes were studied after subjecting cells to two different HSs. Our results suggest that, under moderate HS, the redox homeostasis is mainly guaranteed by an increase in glutathione (GSH) content and in the ascorbate peroxidase (APX) and catalase (CAT) activities. These two enzymes undergo different regulatory mechanisms. On the other hand, the HS‐induced PCD determines an increase in the activity of the enzymes recycling the ascorbate‐ and GSH‐oxidized forms and a reduction of APX; whereas, CAT decreases only after a transient rise of its activity, which occurs in spite of the decrease of its gene expression. These results suggest that the enzyme‐dependent ROS scavenging is enhanced under moderate HS and suppressed under HS‐induced PCD. Moreover, the APX suppression occurring very early during PCD, could represent a hallmark of cells that have activated a suicide programme.