Influence of jasmonic acid on endogenous gibberellin and abscisic acid in salt-stressed chard plant.

The endogenous gibberellin (GA) and abscisic acid (ABA) contents as an effect of different application times of jasmonic acid (JA) in chard seedlings exposed to salt stress were investigated. Endogenous ABA content was increased by JA treatment after NaCl treatment, rather than after JA application before NaCl treatment. JA application after NaCl treatment caused higher ABA content than treatment with 160 mM NaCl alone. Total gibberellin content decreased after NaCl stress, but NaCl-reduction in total GA contents counteracted by exogenous JA. Total endogenous GA contents were increased in JA treatment after NaCl and were highest at 24 hr of JA application before NaCl exposure. JA treatment promoted the increase of dry weight compared to chard plant exposed to 160 mM NaCl. Thus, JA presumably induces gibberellin biosynthesis showing the promotion of growth and dry weight of chard plants under salt stress.

Agmatine pretreatment protects retinal ganglion cells (RGC-5 cell line) from oxidative stress in vitro

Agmatine, 2-(4-aminobutyl)guanidine, has been reported to have neuroprotective effects against various neuronal damages. In this study it was investigated whether agmatine pretreatment rescues the retinal ganglion cells from oxidative injury in vitro. Alter differentiation of transformed rat retinal ganglion cells (RGC-5 cell line) with staurosporine, agmatine (0.0 to 100.0 microM) pretreatment was performed for 2 hours. Subsequently, they were exposed to hydrogen peroxide (0.0 to 2.5 mM) as an oxidative stress. Cell viability was monitored for up to 48 hours with the lactate dehydrogenase (LDH) assay and apoptosis was examined by the Terminal deoxynucleotide transferase-mediated terminal uridine deoxynucleotidyl transferase nick end-labeling (TUNEL) method. As a result, differentiated RGC-5 cells were found to have decreased viability after addition of hydrogen peroxide in a dose-dependent manner. This hydrogen peroxide induced cytotoxicity caused apoptosis characterized by DNA fragmentation. Agmatine pretreatment not only increased cell viability but also attenuated DNA fragmentation. In conclusion, agmatine pretreatment demonstrated neuroprotective effects against oxidative stress induced by hydrogen peroxide in differentiated RGC-5 cells in vitro. This suggests a novel therapeutic strategy rescuing retinal ganglion cells from death caused by oxidative injury.