Carbonization products C1, C2, C3, C4 and C5 were prepared by the carbonization of date pit in limited air, at 500, 600, 700, 800 and 1000℃, respectively. C1-V-600, C3-V-600, C1-V-1000 and C3-V-1000 were prepared by thermal treatment of C1 and C3 under vacuum at 600 and 1000℃. The textural properties were determined from nitrogen adsorption at 77 K and from carbon dioxide adsorption at 298 K. The surface pH, the FTIR spectra and the acid and base neutralization capacities of some carbons were investigated. The amounts of surface oxygen were determined by out-gassing the carbon-oxygen groups on the surface as CO2 and CO. The adsorption of water vapor at 308 K on C1, C2, C3 and C4 was measured and the decomposition of H2O2 at 308 K was also investigated on C1, C2, C3, C4 and C5. The surface area and the total pore volume decreased with the rise of the carbonization temperature from 500 to 1000℃. The adsorption of water vapor is independent on the textural properties, while it is related to the amount of acidic carbon-oxygen groups on the surface. The catalytic activity of H2O2 decomposition does not depend on the textural properties, but directly related to the amount of basic carbon-oxygen complexes out-gassed as CO, at high temperatures.

홍삼의 추출물인 50% ethanol extract, crude saponin, 그리고 lipid soluble fraction이 마우스 대식세포의 oxidative burst를 유발할 수 있는지 여부를 알아보고자 in vitro와 in vivo에 각각의 추출물을 처치하고 hydrogen peroxide 생산을 DCFH-DA를 이용한 형광분광광도법으로 측정하였다. 형광분광법에 의한 hydrogen peroxide의 측정을 최적화하기 위한 DCFH-DA의 농도는 3.2 μM이었고, oxidative burst를 유발하지 못하였지만, zymosan A로 유발한 경우에는 50% ethanol extract에서 가장 높은 hydrogen peroxide를 생산하였다. In vivo 실험에서는, lipid soluble extract에서만 유의하게 증가한(P<0.01) oxidative burst를 유발하였고, ginsenoside(saponin)가 어느 정도 포함되어 있는 50% ethanol extract와 crude saponin은 대조군에 비하여 유의하게 낮은(P<0.05) hydrogen peroxide를 생산하였다. 이는 ginsenoside가 마우스의 nitric oxide 생산을 억제한다는 다른 연구자들의 보고와 일치하는 결과이다. Oxidative burst를 유발한 lipid soluble extract에는 phenol계 화합물, polyacetylene계 화합물, 미량선분 등이 함유되어 있으므로 차후 연구를 통하여 과연 어느 성분이 hydrogen peroxide를 증가시키는지를 규명하는 것이 필요하다.

Bioremediation in situ is heavily dependent on the oxygenic environment which would privide the dwelling microorganism with sufficient oxygen. The situation could be easily resolved with supply of an Oxygen Releasing Compound (ORC). In this paper we prepared that sort of material out of oyster shell powder (mostly calcium carbonate) that prevails every shore areas of the country. We used two different oxidizing methods in the first step of the whole manufacturing process–conventional heating in a furnace and an ultrasound generator to obtain calcium oxide. Then that calcium oxide was further oxidized into calcium peroxide which may release oxygen under a moisturized condition. The oxygen releasing experiments were run to test the performance of our products, and to determine the gas kinetics during the experiments. Interestingly, calcium peroxide derived from ultrasound treatment was much more energy-effective as ORC than that from furnace heating although the heat derived process was better than that of ultrasound in terms of oxygen content and its releasing rate. We also found that most of the data collected from the gas releasing experiments fairly supported an ordinary 1st order kinetics to oxygen concentration, which shaped a sharp discharge of oxygen at the very early moment of each test.

Background : Cellular oxidative stress as reactive oxygen species (ROS), whether produced endogenously as a consequence of normal cell functions or derived from external sources, pose a constant threat to cells living in an aerobic environment as they can result in severe damage to DNA, protein, and lipids. The effects of Valeriana fauriei extract and fractions on hydrogen peroxide-induced neuronal cell damage are studied. Methods and Results : Oxidative stress plays an important role in the pathological process of neurodegenerative diseases. Valeriana fauriei extract (VFE) and EA fractions (VFEA) was investigated total phenolic contents using method. VFE of total phenolic contents had 2.54 ± 0.01 mg/g, also, VFEA had a 18.78 ± 0.03 mg/g. High phenolic content of the VFEA is expected to better the inhibition of oxidative stress. VFE and VFEA were experimented to inhibit ROS induced 200 μM 3-morpholinosydnonimine (SIN-1). VFE of inhibit SIN-1 induced-ROS dose dependently and signficantly. In addition, VFEA inhibition was also dose dependant and significant. Moreover, The treatment of SH-SY5Y and SK-N-SH cells with VFEA significantly reduced hydrogen peroxide-induced generation of intercellular ROS. Conclusion : From the above results, we may suggest that VFEA might have useful as a material for functional food and pharmaceutics for the pathological process of neurodegenerative diseases.

Mussels are stubborn organism attached to solid substrate by byssus threads and caused operational problems in utility of power generating stations. Sole and combined usage of ultrasonic (28 kHz- and 42 kHz- frequencies) and hydrogen peroxide (H2O2) has studied for control of blue mussel larvae and adult stage in seawater condition. A theoretical wo rking model using disinfection (Chick and Watson type) approaches is presented based on helpful results of experiments. This study also demonstrate that the combined treatment (ultra-sonication with H2O2) is overall highly efficient than individual treatment would, but on the basis of exposure time, the ultra-sonication was the most efficient among them. Therefore the development of sole and combined technique might be effective practical mitigation strategy against mussel attachment for water handling facilities.

Background : Reactive oxygen species (ROS), whether produced endogenously as a consequence of normal cell functions or derived from external sources, pose a constant threat to cells living in an aerobic environment as they can result in severe damage to DNA, protein, and lipids. The effects of Valeriana fauriei extract and fractions on hydrogen peroxide-induced neuronal cell damage are studied. Methods and Results : Oxidative stress plays an important role in the pathological process of neurodegenerative diseases. Valeriana fauriei extract (VFE) and EA fractions (VFEA) was investigated total phenolic contents using method. VFE of total phenolic contents had 2.54 ± 0.01 mg/g, also, VFEA had a 18.78 ± 0.03 mg/g. High phenolic content of the VFEA is expected to better the inhibition of oxidative stress. VFE and VFEA were experimented to inhibit ROS induced 200 μM 3-morpholinosydnonimine (SIN-1). VFE of inhibit SIN-1 induced-ROS dose dependently and signficantly. In addition, VFEA inhibition was also dose dependant and significant. Moreover, Treatment of SH-SY5Y and SK-N-SH cells with VFEA significantly reduced hydrogen peroxide-induced generation of intercellular ROS. Conclusion : From the above results, we may suggest that VFEA might have useful as a material for functional food and pharmaceutics for the pathological process of neurodegenerative diseases.

오디 당침출액(MSE)의 산화적 스트레스 개선 효과를 확인하기 위하여 HepG2 세포에 H2O2로 산화적 스트레스를 유도시킨 다음, MSE의 보호효과를 확인하였다. MSE를 40 일간 저장하여 DPPH radical scavensing을 통해 DPPH radical 소거능이 유의적으로 좋았던 저장 40일용 MSE를 선택하여 세포 실험에 적용하였다. HepG2 세포에 500 μM H2O2를 처리하여 산화적 스트레스를 유발시키고, MSE를 처리하여 세포 생존율을 확인한 결과, MSE 처리로 인한 세포 생존율이 유의적으로 증가하였고, ROS 생성과 과산 화물에 대한 지표로 측정된 MDA 농도도 MSE 처리로 인해 효과적으로 억제되었다. 또한, H2O2 처리로 감소된 SOD 및 CAT 활성이 MSE 처리로 인해 유의적으로 높아졌으며, H2O2를 처리로 인한 세포핵의 apoptosis body가 MSE 처리 로 인해 감소함을 확인하였으며, 이는 caspase-3 활성 MSE 가 억제시킴으로 인해 세포를 보호하고 있음을 확인하였 다. 이상의 결과로부터 오디 당침출액은 산화적 스트레스 로부터 야기되는 세포독성과 apoptosis로부터 세포 보호 효과를 확인함에 따라 향후 노화와 관련된 다양한 연구 소재의 기초 자료 및 질병 예방 소재로의 가능성을 확인하 였다.

Development and performance evaluation of the hydrogen generator by autothermal reforming process for emergency PEM fuel cell using methanol from process waste were carried out. Supply of gaseous hydrogen has been a technical barrier for its wide application. As a result, conventional reformer has either a separate heat source such as a catalytic combustor or a parallel process in the same reactor to generate heat. The later device is called ATR (Autothermal reforming). Typical product gas of ATR still contains a large amount of carbon monoxide that poisons electro-catalyst of the MEA. In the present study, we used the decomposition of hydrogen peroxide as a parallel exothermic reaction in the same reactor as the reformer. The decomposition of hydrogen peroxide releases water vapor and gaseous oxygen with enormous heat. The heat sustains the reforming reaction and the oxygen is used to recombine the carbon monoxide by oxidation. By parametric study, at the condition of 200oC and the rate of methanol to 40% of hydrogen peroxide is 4 to 1, the Carbon monoxide contents are reduced by less than 800 ppm. Using the present concept we could reduce the concentration of carbon monoxide in the product gas of the reformer by more than 80%. At that carbon monoxide contents, we can be possible to load the methanol-hydrogen peroxide ATR system without any devices.

In this study, the effect of hydrogen peroxide (H2O2) pre-treatment for sewage sludge prior to anaerobic digestion wasassessed using a batch test with an objective to decrease nitrogen, dissolved sulfide and siloxane in sewage sludge. Atotal of 6 sets of experiments (Blank, 20, 40, 60, 80 and 100g H2O2/kg wet sludge) were carried out, each with duplicates.To assess the effect of different dosages of H2O2 on anaerobic digestion, the treated sewage sludge was used for biochemical methane potential (BMP) test and SCODcr concentration. Due to the H2O2 pre-treatment, solubilization of SCODcr in pretreated sludge increased by 89% compared to raw sewage sludge, whereas T-N and NH3-N concentrationdecreased. Cumulative methane yields were increased for all pretreated samples due to increased sludge solubilizationthrough H2O2 pre-treatment. In addition, dissolved siloxane concnetrations were decreased for all pretreated samples. Thus,a reduction in dissolved siloxane concenrtation can decrease the siloxane generation potential of sludge during anaerobicdigestion. However, dissolved sulfide concentration remained same. Although H2O2 dosage did not show any furtherimpact on dissolved sulfide, they have significantly decreased T-N, NH3-N and dissolve siloxane concentrations beforeanaerobic digestion.

활성산소의 하나인 과산화수소(hydrogen peroxide, H2O2)에 대한 세포독성과 이에 대한 연꽃수술(Nelumbo nucifera stamen, NNS)추출물의 항산화효과 및 멜라닌화에 미치는 영향을 알아보기 위하여 세포부착율 (cell adhesion activity, CAA)을 비롯한 티로시나제활성저해능 및 총멜라닌합성량을 분석하였다. 본 실험 결과 hydrogen peroxide(H2O2)는 배양 인체피부흑색종세포 (SK-MEL-3)의 CAA를 유의하게 감소시킴으로서 세포독성효과를 나타냈다. 이에 대하여 NNS추출물은 H2O2의 산화적 손상에 의하여 감소된 CAA를 유의하게 증가시킴으로서 항산화효과를 나타냈다. 한편, H2O2에 대한 NNS추출물의 멜라닌화에 대한 영향에 있어서 NNS추출물은 H2O2에 의하여 활성화된 티로시나제활성과 총멜라닌합성량을 감소시킴으로서 멜라닌화에 대하여 억제효과를 나타냈다. 이상의 결과로 부터 H2O2는 배양 인체피부흑색종세포에 고독성을 나타냈으며 NNS와 같은 식물추출물은 H2O2와 같은 활성산소에 의한 산화적 손상 및 멜라닌화를 방어하는데 효과적인 것으로 나타났다.

산소자유라디칼의 하나인 hydrogen peroxide(H2O2)에 대한 세포독성과 이에 대한 페놀화합물의 일종인 gallic acid의 영향을 cell adhesion activity(CAA)를 비롯한 DPPH-radical scavenging activity, lactate dehydrogenase(LDH) activity에 의하여 분석하였다. 본 실험에서 H2O2는 배양 인체피부흑색종세포(SK-MEL-3)에 처리한 농도에 의존적으로 유의한 세포부착율의 감소를 나타냈으며 또한 고독성 효과를 보였다. 한편, H2O2의 산화적 손상에 대한 gallic acid의 방어효과를 조사하기 위하여 세포부착율과 LDH 활성을 조사하였다. 그 결과 gallic acid는 H2O2에 의하여 감소된 세포부착율을 유의하게 증가시킨 반면, LDH 활성은 유의한 감소를 보임으로서 항산화효과를 나타냈다. 더욱이 gallic acid는 DPPH-radical scavenging activity의 분석에서 유의한 자유라디칼 소거능을 보였다. 이상의 결과로 부터 H2O2는 배양 인체피부흑색종세포에 고독성을 나타냈으며 gallic acid와 같은 페놀화합물은 H2O2와 같은 산화적 손상을 방어하는데 효과적이었다.

Vitis amurensis (VA; Vitaceae) has long been used in oriental herbal medicine. It has been reported that roots and seeds of VA have anti-inflammatory and antioxidant effects. In the present study, the protective effect of ethanol extract from stems and leaves of VA on hydrogen peroxide (H2O2) (100 μm)-induced neuronal cell damage was examined in primary cultured rat cortical neurons. VA (10-100 μg/ml) concentration-dependently inhibited H2O2-induced apoptotic neuronal cell death measured by 3-[4,5-Dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and Hoechst 33342 staining. VA inhibited H2O2-induced elevation of intracellular Ca2+ concentration ([Ca2+]i) and generation of reactive oxygen species (ROS), which were measured by fluorescent dyes. Pretreatment of VA also prevented glutamate release into medium induced by 100 μm H2O2, which was measured by HPLC. These results suggest that VA showed a neuroprotective effect on H2O2-induced neuronal cell death by interfering with H2O2-induced elevation of [Ca2+]i, glutamate release, and ROS generation. This has a significant meaning of finding a new pharmacological activity of stems and leaves of VA in the CNS.

본 연구는 활성산소종의 일종인 hydrogen peroxide(H2O2)에 대한 산수유(Cornus fructus, CF)추출물의 영향을 배양 NIH3T3 섬유모세포를 재료로 세포부착능과 항산화 측면에서 조사하였다. 그 결과 H2O2는 농도 의존적으로 배양 세포의 세포부착능을 감소하였으며 XTT50값이 100 uM이하로 나타남으로서 Borenfreund와 Puerner(1984)의 독성판정기준에 따라 고독성인 것으로 나타났다. 한편, H2O2의 산화적 손상에 대한 CF추출물의 세포부착능에 대한 영향에 있어서 CF추출물의 처리는 H2O2의 산화적 손상으로 감소된 세포부착능을 유의하게 증가시켰다. 또한, H2O2의 산화적 손상에 의하여 유발된 지질과산화에 의한 막손상에 대하여 CF추출물의 처리는 H2O2에 의하여 증가된 LDH 활성을 유의하게 감소시켰다. 또한, CF추출물은 농도 의존적으로 superoxide dismutase(SOD) 유사활성을 나타냈다. 이상의 결과로 부터 H2O2와 같은 활성산소종은 배양 NIH3T3 섬유모세포에 대하여 세포독성을 보였으며 또한 CF추출물은 H2O2에 의한 산화적 손상을 방어함으로서 항산화 효과를 나타냈다.

Bacillus subtilis subsp. subtilis는 녹조류인 매생이에서 분리되는 총 생균주 중에서 90%를 차지하고 있다. Bacillus subtilis subsp. subtilis에 대한 항미생물 활성을 50 ppm 수준에서 과산화수소와 NaOCl의 각각의 처리가 전해수 (50 ppm) 보다 유의적 수준에서 높았다. 매생이를 50 ppm의 과산화수소, NaOCl 그리고 전해수로 처리한 후 에서 30일간 일반포장 또는 진공포장에 의한

Dried leaves from Cedrela sinensis A. Juss. (CS), have been observed to possess various pharmacological activity and contain various antioxidant constituents. The protective effect of ethanol extract of CS on hydrogen peroxide (H2O2)-induced neurotoxicity was examined using primary cultured rat cortical neurons in the present study. Exposure of cultured neurons to 100 μM H2O2 caused a significant neuronal death as assessed by a 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and Hoechst 33342 staining. The addition of CS, over a concentration range of 10 to 50μg/ml, concentration-dependently prevented the H2O2-induced neuronal apoptotic death. CS (50μg/ml) significantly inhibited H2O2-induced elevation of the cytosolic Ca2+ concentration ([Ca2+]c), which was measured by a fluorescent dye, Fluo-4 AM. CS (30 and 50μg/ml) inhibited glutamate release and generation of reactive oxygen species (ROS) induced by 100μM H2O2. These results suggest that CS may mitigate the H2O2-induced neurotoxiciy by interfering with the increase of [Ca2+]c, and then inhibiting glutamate release and generation of ROS in cultured neurons.

Plant peroxidases (PODs) have been shown to reduce hydrogen peroxide (H2O2) in the presence of an electron donor. Extracellular POD also induce H2O2 production, and can perform a significant function in responses to environmental stresses. We previously described the isolation of 10 POD cDNA clones from cell cultures of sweetpotato (Ipomoea batatas). Among them, the expression of the swpa4 gene was profoundly induced by a variety of stresses. In this study, transgenic tobacco (Nicotiana tabacum) plants overexpressing the swpa4 gene under the control of the CaMV 35S promoter were generated in order to assess the function of swpa4. Both transient expression analysis with the swpa4-GFP fusion protein and POD activity assays in the apoplastic washing fluid revealed that the swpa4 protein is secreted into the apoplastic space. The transgenic plants also evidenced a significantly enhanced tolerance to a variety of abiotic and biotic stresses. These plants harbored increased lignin and phenolic content, and H2O2 was also generated under normal conditions. Furthermore, they manifested increased expression levels of a variety of apoplastic acidic pathogenesis-related (PR) genes following enhanced H2O2 production. These results suggest that the expression of swpa4 in the apoplastic space functions as a positive defense signal in the H2O2-regulated stress response signaling pathway.

The protective effect of ethanol extract of Korean mistletoe (KM; Viscum album coloratum) on hydrogen peroxide (H2O2)-induced neurotoxicity was examined in primary cultured rat cortical neurons. H2O2 reduced viability of cortical neurons in a concentration-dependent manner. The addition of KM, over a concentration range of 10 to 100 μg/ml, concentration-dependently prevented the H2O2(100 μM)-induced neuronal cell death, as assessed by a 3-[4,5-dimethylthiazol-2-yl]-2,5-di-phenyl-tetrazolium bromide (MTT) assay and Hoechst 33342 staining. KM significantly inhibited H2O2-induced elevation of the cytosolic Ca2+ concentration ([Ca2+]c), which was measured by a fluorescent dye, fluo-4 AM. KM inhibited glutamate release into medium and generation of reactive oxygen species (ROS) induced by H2O2. These results suggest that KM may mitigate the H2O2-induced neurotoxiciy by interfering with the increase of [Ca2+]c, and inhibiting glutamate release and generation of ROS in cultured neurons.