• The Journal of Korean Medicine
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• v.22 no.3
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• pp.63-73
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• 2001

Objectives : The objective of the current study is to determine the protective effect of Ukyium(Yougui-yin) on the apoptosis induced by zinc. Methods : Zinc is known to generate reactive oxygen species (ROS), including superoxide anion ($O_2$) and hydrogen peroxide ($H_2O_2$), which eventually contribute to cytotoxicity in a variety of cell types. We investigated the viablity of cells, $H_2O_2$ generation, chromatin condensation and nuclear fragmentation in Hoechst dye staining and $IkB-{\alpha}$ degradation in C6 glial cells of $ZnCl_2$ between pretreatment- and not pretreatment-group with Ukyium. The former methods were researched by Time- and Dose-dependent manners. Results : We demonstrated that pretreatment with Ukyium prevented zinc-induced cell death of C6 glial cells and apoptotic characteristics including chromatin condensation and nuclear fragmentation. Ukyium also prevented $H_2O_2-induced$ cell death. We further confirmed that Ukyium decreased zinc-induced generation of $H_2O_2$ and inhibited degradation of $IkB-{\alpha}$ by zinc in C6 glial ceHs. Conclusions : These data indicated that Ukyium (Yougui-yin) prevents zinc-induced apoptotic death of C6 glial cells via inhibition of ROS generation, such as $H_2O_2$ as well as inhibition of $IkB-{\alpha}$ degradation.

• Archives of Pharmacal Research
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• v.22 no.1
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• pp.35-43
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• 1999

Overstimulation of both kainate (KA) and N-methyl-D-aspartate (NMDA) receptors has been reported to induce excitatoxicity which can be characterized by neuronal damage and formation of reactive oxygen free radicals. Neuroprotective effect of melatonin against KA-induced excitotoxicity have been documented in vitro and in vivo. It is, however, not clear whether melationin is also neuroportective against excitotoxicity mediated by NMDA receptors. In the present work, we tested the in vivo protective effects of striatally infused melatonin against the oxidative stress and neuronal damage induced by the injection of KA and NMDA receptors into the rat striatum. Melatonin implants consisting of 22-gauge stainless-steel cannule with melatonin fused inside the tip were placed bilaterally in the rat brain one week prior to intrastriatal injection of glutamate receptor subtype agonists. Melatonin showed protective effects against the elevation of lipid peroxidation induced by either KA or NMDA and recovered Cu, Zn-superoxide dismutase activities reduced by both KA and NMDA into the control level. Melatonin also clearly blocked both KA- and NMDA-receptor mediated neuronal damage assessed by the determination of choline acetyltransferase activity in striatal monogenages and by microscopic observation of rat brain section stained with cresyl violet. The protective effects of melatonin are comparable to those of DNQX and MK801 which are the KA- and NMDA-receptor antagonist, respectively. It is suggested that melatonin could protect against striatal oxidative damages mediated by glutamate receptors, both non-NMDA and NMDA receptors.

• Journal of Life Science
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• v.11 no.3
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• pp.279-283
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• 2001

Amyotrophic lateral sclerosis(ALS) is a progressive neurologic disorder resulting from the degeneration of upper and lower motor neurons, and is inherited in 10% of cases. About 20% of familial ALS, clinically indistinguishable from sporadic ALS, is caused by mutations of Cu/Zn superoxide dismutase on chromosome 21q22.21 inherited as an autosomal dominant trait. We now report a new locus in the non-SOD1 dominantly inherited ALS. We screened a large ALS family with 11 affected individuals and one obligate gene carrier with genome-wide ABI polymorphic markers using the ABI 377 automated system. No evidence of linkage was obtained with the autosomal markers. We next screened this family with X chromosome markers as there was no evidence of male-to-male tran-smission of the disease. Linkage was established with several X chromosome markers with a lod score up to 3.8; almost the maximum possible score in this family. Our finding imply that a gene for the dominant expression of a neuronal degeneration is coded on X chromosome and raise the question of the role of X-linked genes that escape inactivation in this pathogenesis. More importantly, our finding that a gene causing ALS is localized on X-chromosome has direct investigational relevance to sporadic ALS, where epidemiological studies show male gender predominance(1.3:1) and earlier onset in men by 5-10 years.

• Journal of the Korean Society of Tobacco Science
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• v.18 no.2
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• pp.160-169
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• 1996

Effect of cigarette smoke exposure on 1-methyl-4-phpnyl-1,2,3,6-tetrahydro-pyidine (Mm)-induced neurotoxicity was investigated in C57BL6 mice. Cigarette smoke exposure of mice to the mainstream smoke generated from 15 cigarettes for 10 mins per day, 5 days per week, for fi weeks, effectively attenuated the decline both in the level of striatal dopamine and the number of brrosine hydros:ylase-positive ceils in the brain caused by MPTP treahent. Exposure to cigarette smoke significantly decreased monoamine oxidate B activity in the cerebral cortex and cerebellum. The activity of brain antioxidant enzymes such as catalase, glutathione peroxidase, and Cu, Zn-superoxide dismutase, was not changed by cigarette smoke exposure or MPTP treatment. Sulfhydryl compounds content in all brain regions except for the striatum was uniquely increased by MPTP treatment, however, such an effect of MPTP was not observed in mice exposed to cigarette smoke. These results suggest that cigarette smoke exposure inhibits MPTP-induced neurotoxicity without influencing free radical metabolism in the brain of mice. This protective effect of cigarette smoke seems to be closely related with the decreased activity of brain monoamine oxidase H. Key words : cigarette smoke exposure, dopamine, monoamine oxidase B, antioxidant enzywles, MPTP.

• The Korean Journal of Ecology
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• v.26 no.3
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• pp.115-121
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• 2003

Leaves of two-week old seedlings of tomato (Lycopersicon esculentum) were treated with various concentrations (0∼100 M) of $CdCl_2$ for up to 9 days and subsequent growth of seedlings, symptoms of oxidative stress and isozyme activities of antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX) and peroxidase (POX) were investigated. Compared with the non-treated control, Cd exposure decreased biomass but increased Cd accumulation, hydrogen peroxide production and lipid peroxidation as malondialdehyde (MDA) formation in leaves and roots. Further studies on the developmental changes of isozyme activities showed that Fe-SOD, Cu/Zn-SOD and one of three APX isozymes decreased and CAT and one of four POX isozymes increased in leaves, whereas Fe-SOD, one of three POX isozymes and two of four APX isozymes decreased and CAT increased in roots, showing different expression of isozymes in leaves and roots with Cd exposure level and time. Based on our results, we suggest that the reduction of seedling growth by Cd exposure is the oxidative stress resulting from the over production of $H_2O_2$ and the insufficient activities of antioxidant enzymes particularly involved in the scavenging of $H_2O_2$. Further, the decreased activities of SOD and APX isozymes of chloroplast origin, the increased activities of CAT and POX and high $H_2O_2$ contents with Cd exposure might indicate that Cd-induced oxidative stress starts outside chloroplast.

• Journal of Nutrition and Health
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• v.40 no.2
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• pp.111-117
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• 2007

This study was designed to investigate the effects of pyroligneous liquor on oxygen radicals and their scavenger enzymes in the liver of Cri/Bgi CD rats (7 rats per group). Male rats were fed a basic diet prepared in our Lab., PL-0 (Control), PL-1, PL-25, PL-50 and PL-75 groups were Prepared to be 0%, 1%, 25%, 50% and 75%with distilled water using pyroligneous liquor (35% of Choa Co. Ltd.), and were administrated orally for 8 weeks. Superoxide radical contents in liver mitochondria and microsomes were significantly decreased to 12-14%, 11-15%, respectively, in these PL-25 and PL-50groups compared with the control group. Hydroxyl radical content in mitochondria and microsomes were markedly decreased to 12-20% and 17%, respectively, in these PL-25 and PL-50% groups compared with the control group. Hydrogen peroxide content in mitochondria and microsomes were significantly decreased about 15-12% and 22-20% in liver of PL-25 and PL-50 groups compared with the control group. Mn-SOD and Cu/Zn-SOD activities in liver of PL-25 and PL-50 groups were remarkably increased to 15-25%, 11-16%, respectively, compared with the control group. GPx activities in mitochondria and microsomes were significantly increased in the liver of PL-25 and PL-50 groups compared with the control group. CAT activities in mitochondria and cytosol were significantly increased to 12-14%, 15-27%, respectively, in the liver of PL-25 and PL-50 groups compared with the control group. These results suggest that long term administration orally of 25 and 50% pyroligneous liquor may effectively inhibit the formation of oxygen free radicals, and also scavenger enzyme activities significantly increase through the administration orally.

• Molecules and Cells
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• v.20 no.3
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• pp.401-408
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• 2005

Reactive oxygen species (ROS) contribute to the development of various human diseases. Cu,Zn-superoxide dismutase (SOD) is one of the major means by which cells counteract the deleterious effects of ROS. SOD activity is dependent upon bound copper ions supplied by its partner metallochaperone protein, copper chaperone for SOD (CCS). In the present study, we investigated the protective effects of PEP-1-CCS against neuronal cell death and ischemic insults. When PEP-1-CCS was added to the culture medium of neuronal cells, it rapidly entered the cells and protected them against paraquat-induced cell death. Moreover, transduced PEP-1-CCS markedly increased endogenous SOD activity in the cells. Immunohistochemical analysis revealed that it prevented neuronal cell death in the hippocampus in response to transient forebrain ischemia. These results suggest that CCS is essential to activate SOD, and that transduction of PEP-1-CCS provides a potential strategy for therapeutic delivery in various human diseases including stroke related to SOD or ROS.

• Journal of Korean Biological Nursing Science
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• v.3 no.1
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• pp.41-52
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• 2001

This study was undertaken to investigate the effects of n-6(corn oil) & n-3(fish oil) fatty acids on infarction size and the cerebral activities of antioxidant enzyme in rat focal brain ischemia model. Weaning Sprague-Dawley rats were fed with either corn oil supplemented diet(COD, 14% corn oil) or fish oil supplemented diet(FOD, 14% menhaden oil) for 6 weeks. The right middle cerebral artery was occluded for 2 hours with a silicon rubber coated nylon surgical thread. After 24 hours of recirculation, the rats were sacrificed and brain sections were photographed using CCD camera after staining with 2, 3, 5-triphenyltetrazolium chloride for 60 minutes in room temperature. The infarcted area was measured and the volume of infarction was calculated. Catalase(CAT), superoxide dismutase(SOD) activities, and fatty acid composition in the brain were also measured. The total and corrected infarction volumes were not significantly different between FOD and COD group. The docosagexaenoic acid(DHA) and DHA content/arachidonic acid(AA) ratio of the cerebral cortex, an index of defense against lipid oxidation, were significantly increased in FOD group compared to those of COD group(p<0.05). In the left cortex(non-infarction side) as well as the right cortex(infarction side) of FOD group, CAT and Cu/Zn SOD activities were higher than those of the COD group(p<0.05). However, CAT and Cu/Zn SOD activities were not significantly different between the left cortex(non-infarction side) and the right cortex(infarction side) of both FOD and COD group. GPx activities were also not significantly different between two groups. Our results demonstrate that the brain infarction size in FOD and COD were not significantly different. However, cerebral lipid composition and antioxidant enzyme activities in FOD and COD group were different. Fish oil, a source of n-3 polyunsaturated fatty acid(PUFA) and corn oil, that of n-6(PUFA) may have a protective effect against oxidative stress induced via different mechanisms.

• Korean Journal of Acupuncture
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• v.36 no.1
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• pp.63-73
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• 2019

Objectives : This study was designed to investigate the effects of Alismatis Rhizoma (AR) pharmacopuncture at BL23 on acute renal failure induced by cisplatin. Methods : The Sprague-Dawley rats were divided into Normal group (no injection of cisplatin and no treatment), Control group (cisplatin injection without treatment), Acu group (needling at BL23 after cisplatin injection), AR-PA1 group (treated with $0.3571mg/kg/20{\mu}l$ of AR pharmacopuncture at BL23 after cisplatin injection), and AR-PA2 group (treated with $1.7855mg/kg/20{\mu}l$ of AR pharmacopuncture at BL23 after cisplatin injection). Each treatment was given once daily for 8 days. Changes in body weight, kidney weight, tumor necrosis factor-alpha ($TNF-{\alpha}$), interleukin-6 (IL-6), Cu-Zn superoxide dismutase (Cu-Zn SOD), glutathione peroxidase (GPx), serum blood urea nitrogen (serum BUN), and serum creatinine were observed. Results : Body weight was significantly increased in AR-PA1 on $4^{th}$ and $6^{th}$ days and AR-PA2 on $2^{nd}$ day. $TNF-{\alpha}$ was significantly decreased in Acu, AR-PA1 and AR-PA2 groups. Cu-Zn SOD was significantly increased in AR-PA2 group. GPx was significantly increased in AR-PA1 and AR-PA2 groups. But kidney weight, IL-6, serum BUN and serum creatinine were not significantly changed in any groups compared to control group. Conclusions : In acute renal failure induced by cisplatin, AR pharmacopuncture has a mitigating effect on the inflammatory reaction related to the increase of $TNF-{\alpha}$ in the kidney tissue and a protective effect on the oxidative stress of the kidney tissue. However it is unlikely to restore the glomerular function or inhibit the renal swelling.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.33 no.2
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• pp.87-92
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• 2000

This study was designed to investigate the effects og $10{\%},\;20{\%}\;and\;40{\%}$-addition of functional brown algae (FBA)-noodles on oxygen radicals and their scavenger enzymes in liver of Sprague-Dawley(SD) male rats. Hydroxyl radicals$({\cdot}OH)$ formations were significantly inhibited$(20{\~}35{\%}\;and\;12{\~}20{\%})$ in liver mitochondria and microsomes of rats administered $0{\%},\;20{\%}\;and\;40{\%}$ FBA-noodles compared with that of control group. Significant differences in $H_2O_2$ formations of liver microsome in these FBA-noodles fed groups could not be obtained, but superoxide-radical $(O_2^({\cdot}-))$ formations of liver cytosol resulted in a significant decrease about $10{\%}\;in\;20{\%}\;and\;40{\%}$ FBA-noodles compared with control group. Mn-SOD activities in liver mitochondria were significanlty increased $(10{\~}15{\%})$ in the groups fed $10{\%},\;20{\%}\;and\;40{\%}$ FBA-noodles, while a group administered $40{\%}$ FBA-noodle only resulted In a significant increases $(about 12{\%})$ in Mn-SOD activity of liver microsomes compared with control group. Cu, Zn-SOD activities in liver cytosol were significantly increased $(10{\~}20{\%})\;in\;10{\%},\;20{\%}\;and\;40{\%}$ FEA-noodles compared with control group. Administration of $10{\%},\;20{\%}\;and\;40{\%}$ FBA-noodles resulted in a marked increases$(20{\~}40{\%})$ in liver cytosolic glutathione peroxidase (GSHPx) compared with control group. Significant differences in lipid peroxide (LPO) levels of mitochondria and microsomes in $10{\%}$ FBA-noodle could not be obtained, while LPO levels of $20{\%} and 40{\%}$ FBA-noodles were significantly inhibited about $10{\%}$ in mitochondria and microsomes compared with control group. These results suggest that these FBA-noodles may play a desirable role in attenuating an oxygen radical formations and increasing a scavenger enzymes activity by some brown algae (Undaria pinnatifida) components.