The nitric oxide(NO) is a major factor contri buting to t he loss of neurons in ischemic st roke. demyelina t ing diseases, and other neurodegenerative di sorders . But it is known that NO is not function ing as a direct neurotoxin. NO combined with superoxide(02-) by the diffusion-contl'O ll ed reaction, formed a peroxin it ri te anion (ONOO-)‘ which this s pecies has been shown to contribute to oxidative s igna ling and damage. ONOO stimuJates apoptosis in many cell types. whether ONOO acts direct ly as an ox idant 0 1' the induction of apoptosis is because of the radicals derived from ONOO- decompositi on . But. the mecha ni sm by which ONOO- induces apoptosis is un clear although subsequent forrnation 0 1' reactive oxygen s pecies(ROS) has been suggested in a few reports The aim of this study is to investigate the a nti -apoptotic pathway by inhibi tion 0 1' ONOO synthesis t hrough scavenging of ROS us ing s pecific wavelength 0 1' light irradiation . The present study investi gated the a nti -apop totic effect of the specific wavelength 0 1' irradi ation in Sodium Nitroprusside(SNP) t reated SJ-I-SY5Y ceJls, by MTT, DNA fragmentation, and flow cytometric assay and th rough western blot and caspase-3, -9 activity assay for confirmation of caspase pathway. Also. NO reJease and ROS leveJ was measured in order to observe the changes of NO involved in radical by Griess reaction analysis and DCF'-DH. Results showed that the cell viability were r educed by about 50% of control group by SNP treatment, but re covered to about 80% by 590nm irradiation . The apoptotic cells were observed by flow cytomet ry and DNA fra g mentation assay in SNP-treated group‘ but 590nm irradiation led apoptotic feature to be reduced . Released NO a nd ROS level were increased after SNP treatment but ROS level was dec reased in 590nm irradi at ion - treated group, in spite of high NO concentration fo llowing SNP treatment Also. SNP t reatment led cytochrom C release but 590nm irraidiation inhibit it, hence the expression 0 1' caspase-3 and -9 was dec reased sign ificantly‘ These results showed that 590nm irradiation protect neuronal death thl'Ough bl ocking of NO-induced mi tochondri al apoptotic pathway. Also, it suggests that specific wavelength of irradi ation was used for prevent ion from neurodegenerative disordcr progression

We investigated whether sound waves could improve salt tolerance in rice seedling. The rice seedlings were sound treated with 800 Hz for 1hr, and then treated with 0, 75, 150, and 225mM NaCl for 3 days to observe changes in physiological and morphological aspects. Sound treatment seedlings resulted in enhanced salt stress tolerance, mainly demonstrated by the sound treated seedlings exhibiting of increased root relative water contents (RWC), root length and weight, photochemical efficiency (ratio of variable to maximum fluorescence, Fv/Fm), and germination rate under salt stress condition. This demonstrates that a specific sound wave might be used, not only to alter gene expression in plant, but also to improve salt stress tolerance. In order to test the sound’s effect on plant and its contribution in drought tolerance, plants were subjected to various sound frequencies for an hrs. After 24-hrs sound treatment, plants were exposed to drought for next five days. During the experiment it was observed that sound initiated physiological changes showing tolerance in plant. Sound frequency with ≥ 0.8 kHz enhanced relative water content, stomatal conductance and quantum yield of PSII (Fv/Fm ratio) in drought stress environment. Hydrogen peroxide (H2O2) production in sound treated plantwasdeclinedcomparedtocontrol. ThermaCAM (Infra-red camera) a software which was used to analyze the plant images temperature showed that sound treated plant and leaf had less temperature (heat) compared to control. The physiological mechanism of sound frequencies induce tolerance in rice plants are discussed.