Agriculture Reference
In-Depth Information
enon under aerobic conditions (Asada
1999
), signaling regulation of plant metabo-
lism internally, and thereby the growth and development of the plant. A drastic
change in climatic regimes renders the metabolic machinery to re-setup cell internal
molecular profile in charge. This transition costs the leakage of electrons from the
electron flow at the cost of reduction of molecular oxygen in chain. These partially-
reduced oxygen species' are highly reactive and interact with other molecules to
form secondary oxidative free radicals. These free radicals are very toxic if they
accumulate beyond a threshold, so they must be detoxified. These highly reactive
species interact with different components and biomolecules such as enzymes, tran-
scription factors, inhibitor proteins, nucleic acids and membrane lipids, to disrupt
normal metabolic functions. The antioxidation of these species to prevent oxidative
injury is achieved by the schematic array of enzyme systems acting in co-operation
with low molecular weight thiol buffers, better known as antioxidative molecules.
The former one incorporates SOD, APX, GPX, CAT, GRs, while the latter includes
ascorbate (AsA), glutathione (GSH; Noctor and Foyer
1998
; Asada
1999
), proline,
polyamines, etc. Restriction of ROS level within a limit to ensure the survival, and
relative activity of the antioxidant system is important to balance the redox homeo-
stasis for survival and normal growth (Scebba et al.
1999
). This is the reason why
stress tolerance is often interpreted in terms of improved efficiency of antioxida-
tive system in plants. In several studies, it was evidenced that endogenous higher
level of SA deactivates the activity of antioxidant system, while co-operating with
ROS. Furthermore, Kuzniak and Sklodowska (
2005
) have indicated that tomatoes
infected with
B. cineria
, initiate the rise of peroxysomal antioxidant enzyme system
activity, which soon declines with eventual development of disease symptoms.
Research in the last few decades has shown that SA interplays with ROS to sig-
nal genetically-controlled defense reactions, thus activating related genes followed
by progression towards PCD (Overmyer et al.
2003
; Durrant and Dong
2004
; Fob-
ert and Després
2005
; Foyer and Noctor
2005
). The concept of crosstalk between
SA and ROS in defending stress is considered crucial during local and systemic de-
fense responses (Overmyer et al.
2003
; Durrant and Dong
2004
). Initial buildup of
internal SA favours antioxidative defense system (over-expression and activation),
thus altering the activity of regulatory factors through cellular signaling, although
on reaching up to a threshold it becomes suppressive to plant growth metabolism
(Fariduddin et al.
2003
), suggesting oxidation (inactivation) of regulatory factors
and saturation of thiol buffers, and thus suppressing the expression and eventual
activity of antioxidant enzymes and molecules. This results in instant upsurge of
reactive species' and free radicals and subsequent oxidative burst. During the hy-
persensitive responses, the ROS and SA accumulation at higher levels (Pasqualini
et al.
2002
) appears to regulate genetic program in favour of cell death propaga-
tion (Overmyer et al.
2003
). Apoplastic and (Jabs et al.
1996
) mitochondrial burst
of ROS accelerate PCD in synergy (Maxwell et al.
2002
; Dutillent et al.
2003
).
However, there are several other sites and mechanisms of ROS generation (Rao
et al.
1997
; Kawano
2003
). SA has clearly been shown to inhibit the activity of
antioxidant enzymes, namely APX and CAT, leading to over-accumulation of su-
peroxide anion (ROS). SA was shown to block the activity of catalase. This inhi-
