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Lantan and gadolinium inhibited Ca
2+
accumulation in the cells. These inhibitors
suppressed initial phases of electric pulse generation. Ca-chelators, BAPTA and
EGTA, eliminated Ca
2+
content elevation in the cells, but did not interfere with
membrane depolarization, i.e., only Ca
2+
removal from the apoplast is not sufficient
for depolarization; Ca-channels should operate (Kawano et al.
1998
).
4 Conclusions
Salicylic acid is a phenolic compound manifesting many features of phytohor-
mones. This includes numerous physiological responses that depend on its pres-
ence. The spectrum of SA action is wide; therefore, it is very difficult to identify a
single key process determining such diverse effects. There are some reports about
the early action of SA: this is redox balance in the apoplast. This effect was
observed as early as several seconds, when other changes were yet undetectable.
The presence of benzolic ring with several double bonds, hydroxyl and carboxyl
groups allow SA to be involved in redox reactions. In fact, SA addition to the
tobacco cell suspension culture resulted in the formation of superoxide O
2
-
in the
redox reaction with the involvement of H
2
O
2
as an electron acceptor. The accu-
mulation of O
2
2
was suppressed by exogenous SOD converting superoxide into
hydrogen peroxide. In this case, SA served an electron donor. Kawano et al. (
1998
);
Kawano (
2003
); Kawano and Furuichi (
2007
) suggested the following scheme for
this process. SA induces the accumulation of hydrogen peroxide in apoplast by
inhibiting catalase. Electron transfer from guaiacol peroxidase secreted into the
apoplast to H
2
O
2
converts initial form of enzyme (Fe
3+
) into oxidized form (com-
pound-1, Fe
5+
). Compound-1 interacts with SA molecule and is reduced to com-
pound-II (Fe
4+
). As a result the free radical SA' is produced. Transfer of the second
electron from another SA molecule to peroxidase (compound II) returns the enzyme
to the initial form (Fe
3+
) and the second SA-radical is generated. Free SA' radical
reduces molecular oxygen to generate superoxide O
2
2
. The SA devoid of two
electrons on oxidation produces (SA
+
is formed). Thus, in this series of reactions, not
only superoxide is formed but SA is conversed into the free radical enhancing
oxidative burst (Kawano et al.
1998
; Kawano
2003
). Not only guaiacol peroxidase
but also ascorbate peroxidase may be a participant in this process, even though the
latter reaction is very slow. Low SA concentrations do not induce ROS accumulation
leading to the cell death. In contrast, non-toxic elevation of ROS content serves a
signal for the activation of defensive responses in the cell. High SA concentrations
can inhibit antioxidant activity and trigger other processes leading to the cell death.
Sugars are also involved in redox processes in the cells. They enter into metabolic
pathways that generate both ROS (Oxidative Phosphorylation) and the reducing
force NADH and NADPH (oxidative pentose-phosphate pathway), which dissipate
(scavenges) these ROS (Couee et al.
2006
). Another mechanism of interaction
between sugars and redox reactions are non-enzymatic oxidation of hexoses
(autooxidation) (Russell et al.
2002
). Glucose can be oxidized in the presence of
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