The redox gradient across the plasma membrane is a key
indicator of global change and a crucial regulator of redox signalling.
Elevated atmospheric CO2 levels have a stimulating
effect on photosynthesis because of decreased photorespiration,
particularly in C3 plants, which will in turn favour a decline in
photorespiratory H2O2 production relative to oxidative signals
produced by other processes, particularly photosynthetic and
respiratory electron transport (Munne-Bosch et al. 2013). GSH
is an important substrate in the AsA-GSH cycle that acts as a
direct antioxidant and regulator of protein thiol disulphide
redox status (Foyer & Halliwell 1976; Apel & Hirt 2004). GSSG
is usually reduced to GSH by the catalysis of GR. The higher
GR activity induced by elevated CO2 in the heat-stressed
seedlings (Fig. 3) could have been responsible for better turnover
of GSSG to GSH in the tomato genotypes, explaining maintenance of the high GSH/GSSG ratio under elevated CO2
conditions (Fig. 5). Likewise, the higher level of AsA over DHA
resulted in an increased ratio of AsA/DHA (Fig. 5), thereby
maintaining a more reduced redox status under heat stress with
elevated CO2. In alfalfa plants (Medicago sativa L.), ascorbate
was more affected than glutathione by CO2 enrichment, and an
interaction between CO2 and drought prevented a decrease in
the AsA/DHA ratio and increased the GSH/GSSG ratio
compared with ambient CO2 (Sgherri et al. 2000).
In summary, this study demonstrated that heat stress
remarkably damaged the photosynthetic apparatus and caused
oxidative stress, as indicated by the increased levels of MDA
and EL in tomato plants. However, ABA-deficient mutant
(not) tomato seedlings were more sensitive to heat stress, suggesting
a role of endogenous ABA in the adaptation to heat
stress. Interestingly, the elevated CO2 treatment significantly
ameliorated heat-induced damage without altering the endogenous
level of ABA in both genotypes. This CO2-induced heat
stress alleviation is associated with improved antioxidant
capacity, related gene expression and redox homeostasis for an
extended period of time. Thus, it could be concluded that elevated
CO2-induced heat stress tolerance is not dependent on
stimulation of the endogenous ABA level but rather on the
reduction of oxidative stress through the efficient management
of the cellular redox state.