• Proceedings of the Plant Resources Society of Korea Conference
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• 2011.10a
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• pp.14-14
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• 2011

Polyamines (putrescine, spermidine and spermine) play pivotal roles in plant defense to different abiotic and biotic stresses. In order to understand the function of ginseng spermidine synthase gene, a key gene involved in biosynthesis of polyamines, transgenic plant was generated in Arabidopsis. The transgenic plants exhibited high levels of polyamines compared to the untransformed control plants. We investigated the tolerance capacity of transgenic plants to abiotic stresses such as salinity and copper stress. In addition, transgenic plants also showed increased resistance against one of the important fungal pathogens of ginseng, the wilt causing Fusarium oxysporum and one of important bacteria, bacterial blight causing Pseudomonas syringae. However, an activity of the polyamine catabolic enzyme, diamine oxidase (DAO) was increased significantly in F. oxysporum and P. syringae infected transgenic plant. Polyamine catabolic enzymes which may trigger the hypersensitive response (HR) by producing hydrogen peroxide ($H_2O_2$) seem act as an inducer of PR proteins, peroxidase and phenyl ammonium lyase activity. The transgenic plants also contained higher antioxidant enzyme activities, less MDA and $H_2O_2$ under salt and copper stress than the wild type, implying it suffered from less injury. These results strongly suggest an important role of spermidine as a signaling regulator in stress signaling pathways, leading to build-up of stress tolerance mechanisms.

• The Korean Journal of Pharmacology
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• v.30 no.3
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• pp.273-289
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• 1994

Reversible brain ischemia was produced by occluding both common carotid arteries for 5 min, and the effects of aminoguanidine (AG), $DL-{\alpha}-difluoromethylornithine$ (DFMO), MK-801, and nimodipine (NM) on the ischemia induced changes of the polyamine, glutamate and acetylcholine levels in the hippocampus CA1 subfield and the specific $[^3H]\;MK-801$ binding to the hippocampus synaptosomal membranes were studied with a histological reference of the cresyl violet stained hippocampus. The basal putrescine level $(PT:\;74.4{\pm}8.8\;nM)$ showed a rapid increase (up to 1.7 fold) for 5 min of ischemia, remained significantly increased for 6 h, and then resumed the further increase to amount gradually up to about 3 fold 96 h after recirculation. However, the level of spermidine was little changed, and the spermine level showed a transient increase during ischemia followed by a sustained decrease to about 40% of the preischemic level after recirculation. The increase of PT level induced by brain ischemia was enhanced with AG or MK-801, but it was reduced by DFMO or NM. The basal glutamate level $(GT:\;0.90{\pm}0.l4\;{\mu}M)$ rapidly increased to a peak level of $8.19{\pm}1.14\;{\mu}M$ within 5 min after onset of the ischemia and then decreased to the preischemic level in about 25 min after recirculation. And NM reduced the ischemia induced increase of GT level by about 25%, but AG, DFMO and MK-801 did not affect the GT increase. The basal acetylcholine level $(ACh:\;118.0{\pm}10.5\;{\mu}M)$ did little change during/after brain ischemia and was little affected by AG or NM. But DFMO and MK-801, respectively, produced the moderate decrease of ACh level. The specific $[^3H]\;MK-801$ binding to the hippocampus synaptosomal membrane was little affected by brain ischemia for 5 min. The control value (78.9 fmole/mg protein) was moderately decreased by AG and MK-801, respectively but was little changed by DFMO or NM. The microscopic findings of the brains extirpated on day 7 after ischemia showed severe neuronal damage of the hippocampus, particularly CA1 subfield. NM and AG moderately attenuated the delayed neuronal damage, and DFMO, on the contrary, aggravated the ischemia induced damage. However, MK-801 did not protect the hippocampus from ischemic damage. These results suggest that unlike to the mode of anti-ischemic action of NM, AG might protect the hippocampus from ischemic injury as being negatively regulatory on the N-methyl-D-aspartate (NMDA) receptor function in the hippocampus.