Chemistry Reference
In-Depth Information
Fig. 4 Involvement of trace metals in the oxidative abiotic stress responses leading to cell death
in tobacco cells. a Treatment of tobacco cells with three different environmental oxidative
stresses, namely, UVC irradiation (wave length 254 nm, intensity 2.2 mW/cm 2 ), high dose O 3
exposure (concentration 150 ppm), and PAN exposure (0.75 ± 0.15 ppm). b Effects of two metal
chelators against the cell death induction by environmental oxidative stresses. Each environ-
mental stress was applied to Bel-W3 or Bel-B cell suspension for certain length of time as
indicated and statically incubated for 2 h. Then these treated cells were stained with Evans blue
for 1 h and dead cells were counted under microscopes. Evaluation of cell death was repeated for
4 times for each sample. Two chelators, 2 mM 2 0 ,2-bipyridyl (bipy) and 2 mM o-phenanthroline
(o-phen), were added to cell suspension cultures 5 min prior to oxidative treatments. (Left)
Involvement of Fe/Cu under UV-C exposure. (Middle) Involvement of Fe/Cu in O 3 -induced cell
death. (Right) Involvement of Fe/Cu in PAN-induced cell death
molecules. Therefore, generation of HO in the biological systems results in
immediate damages to DNA molecules and the subsequent DNA degradation may
further leads to apoptotic reaction and carcinogenesis in the living cells. Such
oxidative stress-mediated DNA fragmentation and chromosomal dysfunction play
key roles in mammalian cell death mechanisms (Higuchi 2003 ). Therefore, it is
important to seek for the ways to prevent or detoxify the Cu-mediated oxidative
mechanism. Natural chelators of copper such as small peptides reportedly prevent
the degradation of DNA (Yokawa et al. 2011a , b ) and cell death and ROS-stim-
ulated calcium signaling in tobacco cells (Kagenishi et al. 2009 ). Interestingly, SA
might be one of such natural chelators.
Search WWH ::




Custom Search