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against oxidative damage during the early stages of
post-germinative growth in Japanese radish. Similar
increases in the activities of APX and AsA-regenerating
enzymes, MDHAR, DHAR and GR during the course of
germination have also been reported for castor bean
seeds (Klapheck
et al.,
1990) and wheat seeds (Cakmak
et al.,
1993). These observations on SOD activity find
support from several earlier findings concerning the
effects of herbicides (Matters & Scandalios, 1986), air
pollutants (Tanaka & Sugahara, 1980; Lee and Bennett,
1982; Hernandez
et al.,
2000), anoxic and hypoxic stress
(Monk
et al.,
1987; Biemelt
et al.
2000), SO
2
(Madamanchi
et al.,
1994) and salinity (Hernandez
et al.,
1993; Gomez
et al.,
1999; Qureshi
et al.,
2007) on the antioxidant
defence system in plants. The increase in SOD activity
could be a consequence of a
de novo
synthesis of enzymatic
protein (Slooten
et al.,
1995). Methyl viologen (herbicide)
treatment affects the level of chloroplast SOD as well as
mitochondrial cytosolic SODs (Dodge, 1994; Van-Camp
et al.,
1994). Iturbe-Ormaetxe
et al.
(1998) concluded that
the Fe-SOD activity was being inhibited by methyl violo-
gen, but the CuZn- and the Mn-SOD activities were not
being affected. The increase in SOD activity as observed in
the present study with increasing concentrations of insec-
ticidal dose conforms well with the findings of Tsang
et al.
(1991) in
Nicotiana plumbaginifolia
.
Parween
et al.
(2011) evaluated the effect of chlorpy-
rifos on several metabolic and stress-related parameters
of
Vigna radiata
L. Twenty-day-old seedlings were
exposed to several concentrations of chlorpyrifos, rang-
ing from 0 to 1.5 mM, through foliar spraying under
field conditions. Chlorpyrifos increased the lipid peroxi-
dation rate and proline content with a concentration of
1.5 mM by Day 20, whereas dehydroascorbate, and oxi-
dized and total glutathione were increased by 1.5 mM
by Day 10. However, a significant dose-dependent
decline in relation to content of ascorbate, and reduced
glutathione levels were observed at all growth stages.
Among the enzymatic antioxidants, the activities of
superoxide dismutase, ascorbate peroxidase and gluta-
thione reductase were enhanced significantly by all the
concentrations at Day 10. Maximum catalase activity
was observed at Day 10 in controls and declined there-
after. Lipid peroxidation might be the first sign of cellular
membrane damage by organophosphates (Hazarika
et al.,
2003). The significant dose-dependent decrease in
CAT activity observed in the present study at different
stages of plant development is circumstantial evidence
supporting the hypothesis that pesticides cause the
formation of ROS (Farrington
et al.,
1973; Scandalios,
1992, 1993; Sayeed
et al.,
2003; Parvez & Raisuddin,
2005). This could also be due to a flux of superoxide
radicals that are known to inhibit CAT activity (Kono &
Fridovich, 1982). Streb
et al.
(1993) reported similar
changes in CAT activity in Paraquat-treated
Secale cereale
.
Decline in CAT activity is regarded as a general response
to many stresses and is due to inhibition of enzyme
synthesis or change in assembly of the enzyme subunits
(MacRae & Fergusam, 1985; Somashekaraiah
et al.,
1992).
APX activity was relatively low during post-flowering.
APX protects the cell against oxidative damage by detox-
ifying the toxic H
2
O
2
. Increase in APX activity is
suggestive of its role in the detoxification of H
2
O
2
under
insecticide-induced oxidative stress (Morimura
et al.,
1996). Increase in GR activity with increasing
concentration of insecticides could be explained in two
ways: (i) the ascorbate-glutathione cycle might be
operating at a high rate in order to detoxify the ROS in
these plants, or (ii) the reduced glutathione pool has to
be maintained at high levels so that it does not become
limiting for the synthesis of phytochelatins, the small
peptides involved in the sequestration of various metal
ions in the vacuoles (Cobbett, 2000; Stolt
et al.,
2003),
and in the inactivation of pesticides by conjugate
formation. The non-enzymatic cellular antioxidants,
like ascorbate and glutathione, undergo alterations
under oxidative stress (Foyer & Halliwell, 1976; Nakano
& Asada, 1981). We have noted a decrease in the ascor-
bate level under insecticidal stress during the present
investigations. However, the decrease was more
prominent during the post-flowering stage with the
0.20% dose of alphamethrin and deltamethrin and
0.25% dose of lambda-cyhalothrin. Disturbances with
the GSH-independent DHAR or the structural integrity
of MDHAR or the altered activity of PSI as a result of
insecticidal toxicity might be the cause of depletion or
decline of ascorbate (Asc). A decrease in the Asc, pos-
sibly due to shortage of a reductant to maintain the
MDHAR activities, has been reported (Foyer
et al.,
1983). The enhanced levels of GSH in
G. max
due to
insecticidal toxicity suggest an active GSH participation
in the detoxification of oxygen species and free radicals,
directly (non-enzymatic) as well as through certain
enzymes. It is assumed that GSH (Wingate
et al.,
1988)
or GSSG (Winglse & Karpinski, 1996) or a change bet-
ween GSH and GSSG (Foyer
et al.,
1997) may function
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