Programmed Cell Death as a Response to High Light, UV and Drought Stress in Plants - Abiotic Stress: Plant Responses and Applications in Agriculture - page 226

In the last decade a significant progress has been made in improving light-induced oxidative
stress tolerance in plants. Various components of antioxidative system involved in ROS
scavenging have been up- or down-regulated to develop transgenic lines with altered anti‐
oxidants levels. Overexpression of enzymes involved in AsA biosynthesis has been shown
to confer oxidative stress tolerance in tomato plants [158]. Increased AsA content has been
also demonstrated to enhance high light stress tolerance in Arabidopsis [159]. Higher concen‐
tration of GSH has proven to protect potato plants against oxidative damage [160]. More‐
over, reduced level of light-mediated cellular damage has been observed in transgenic
tobacco plants overexpressing chloroplast-localized Cu/Zn-SOD (161) and thylakoid mem‐
brane-bound APX [162]. MDHAR overexpression in Arabidopsis has been demonstrated to
enhance the tolerance towards photooxidative stresses [163]. Moreover, some studies have
reported that combined expression of antioxidant enzymes in transgenic plants acts synerg‐
istically on stress tolerance, e.g. simultaneous overexpression of Cu/Zn-SOD and APX in to‐
bacco chloroplasts enhances the resistance to the photooxidative stress in comparison to
their single overexpression [164].
5. UV radiation stress
Being exposed to sunlight, plants need to deal with the damaging effect of ultraviolet (UV)
radiation which reduces the genome stability, impeding their growth and productivity.
These effects result from damage to cell components including not only nucleic acids, but
also proteins and membrane lipids. Upon UV exposure, strongly mutagenic cross-linked
forms of DNA can be produced [165]. In order to minimize effects of UV radiation, plants
accumulate UV-absorbing secondary metabolites, perform the monomerization of UV-in‐
duced pyrimidine dimers (DNA repair) and neutralize generated ROS [166,167].
UV radiation consists of UV-C (below 280 nm), UV-B (280-320 nm) and UV-A (320-390). Al‐
though UV-C is not physiologically relevant to plants since it is efficiently blocked by the
stratosphere, the UV-C-triggered cell damage is comparable to induced with UV-B radia‐
tion, which reaches Earth's surface [168]. Therefore, UV-C radiation has been widely used to
study DNA damage and repair mechanisms upon UV stress [169].
UV has been demonstrated to trigger apoptosis in animals [170] and apoptosis-like changes
in Arabidopsis , including DNA laddering, changes in nucleus morphology (crescent shape)
and its fragmentation [168]. It has been also proven to induce oxidative burst in plant cells
[171], considered as the main cause of cell death, which aims at the limitation of damage
spreading. Light is necessary for UV-C-triggered cell death and caspase-like proteases par‐
ticipate in this process since caspase-inhibitors are able to block the onset of DNA fragmen‐
tation [25,172]. Recent study performed on Arabidopsis protoplasts has shown that during
the early stage of UV stress, a burst of ROS in chloroplasts and adjacent mitochondria is de‐
tected. Mitochondria dysfunction has been also observed, manifested by changes in their
distribution, mobility and the loss in mitochondrial transmembrane potential. Moreover, the
pre-incubation with antioxidant molecule - ascorbic acid or inhibitor of photosynthetic elec‐