Kim, Nam Hoon;Jeong, Moon Sik;Choi, Soo Young;Kang, Jung Hoon
Molecules and Cells
/
v.22
no.2
/
pp.220-227
/
2006
Oxidative alteration of mitochondrial cytochrome c has been linked to disease and is one of the causes of proapoptotic events. We have investigated the modification of cytochrome c by $H_2O_2$. When cytochrome c was incubated with $H_2O_2$, oligomerization of the protein increased and the formation of carbonyl derivatives and dityrosine was stimulated. Radical scavengers prevented these effects suggesting that free radicals are implicated in the $H_2O_2$-mediated oligomerization. Oligomerization was significantly inhibited by the iron chelator, deferoxamine. During incubation of deoxyribose with cytochrome c and $H_2O_2$, damage to the deoxyribose occurred in parallel with the release of iron from cytochrome c. When cytochrome c that had been exposed to $H_2O_2$ was analyzed by amino acid analysis, the tyrosine, histidine and methionine residues proved to be particularly sensitive. These results suggest that $H_2O_2$-mediated cytochrome c oligomerization is due to oxidative damage resulting from free radicals generated by a combination of the peroxidase activity of cytochrome c and the Fenton reaction of free iron released from the oxidatively-damaged protein.
Optimum temperature and pH of glutamine synthetase activity (E.C. 3.6.1.2.) of R. sphaeroides D-230 was $35^{\circ}C$ and 6.8, respectively. The adenylated state of GS in R. sphaeroides D-230 was stabilized by addition of 0.2mg/ml of cethyltrimethylammoniumbromide. Valine, histidine, proline, isoleucine, and lysine were good nitrogen source for the growth of R. sphaeroides D-230. The growth of R. sphaeroides D-230 in $N_2,\;NaNO_3\;or\;NH_4Cl$ as sole nitrogen source was lower than in any otherculture conditions. GS activity was inhibited, more or less, by various amino acid. THe relative inhibition rate of the enzyme by added 7mM arginine, $NH_4Cl,\;N_2,\;and\;NaNO_3$ was 63.8%, 26.79%, 6.24%, and 10.64%, drespectively. THe hydrogen evolution of R. sphaeroides D-230 grown in N-limited media was inhibited by 0.1mM MSX, irreversible GS inhibitor. GS activity was completely inhibited by 1.0mM MSX but ammonia released maximally at the same concentration of MSX. Ammonia release by added MSX was increased up to 1.0mM MS, but decreased above 1.0mM MSX. It is probably due to inhibition of nitrogenase actixity by MSX. Nitrogenase activity was not inhibited at low concentration of MSX. These results suggests that the inhibition of nitrogenase activity by ammonia is mediated by products of ammonia assimilation rather than by ammonia itself.
Khosa, Muhammad Kaleem;Jamal, Muhammad Asghar;Hussain, Amira;Muneer, Majid;Zia, Khalid Mahmood;Hafeez, Samia
Journal of the Korean Chemical Society
/
v.57
no.3
/
pp.316-321
/
2013
Electrocoagulation (EC) technique is applied for the treatment of wastewater containing heavy metals ions such as nickle (Ni), lead (Pb) and cadmium (Cd) by using sacrificial anodes corrode to release active coagulant flocs usually aluminium or iron cations into the solution. During electrolytic reactions hydrogen gas evolve at the cathode. All the experiments were carried out in Batch mode. The tank was filled with synthetic wastewater containing heavy metals and efficiency of electro-coagulation in combination with aluminum and iron electrodes were investigated for removal of such metals. Several parameters, such as contact time, pH, electro-coagulant concentration, and current density were optimized to achieve maximum removal efficiency (%). The concentrations of heavy metals were determined by using Atomic Absorption Spectroscopy (AAS). It is found that the electro-coagulation process has potential to be utilized for the cost-effective removal of heavy metals from wastewater specially using iron electrodes in terms of high removal efficiencies and operating cost.
Kim, Hyun-Gil;Yang, Jae-Ho;Kim, Weon-Ju;Koo, Yang-Hyun
Nuclear Engineering and Technology
/
v.48
no.1
/
pp.1-15
/
2016
For a long time, a top priority in the nuclear industry was the safe, reliable, and economic operation of light water reactors. However, the development of accident-tolerant fuel (ATF) became a hot topic in the nuclear research field after the March 2011 events at Fukushima, Japan. In Korea, innovative concepts of ATF have been developing to increase fuel safety and reliability during normal operations, operational transients, and also accident events. The microcell $UO_2$ and high-density composite pellet concepts are being developed as ATF pellets. A microcell $UO_2$ pellet is envisaged to have the enhanced retention capabilities of highly radioactive and corrosive fission products. High-density pellets are expected to be used in combination with the particular ATF cladding concepts. Two concepts-surface-modified Zr-based alloy and SiC composite material-are being developed as ATF cladding, as these innovative concepts can effectively suppress hydrogen explosions and the release of radionuclides into the environment.
Licenses for the storage of spent nuclear fuel (SNF) and vitrified highly active waste in casks under dry conditions are limited to 40 years and have to be renewed for prolonged storage periods. If such a license renewal has to be expected since as in accordance with the new site selection procedure a final repository for spent fuel in Germany will not be available before the year 2050. For transport and possible unloading and loading in new casks for final storage, the integrity and the maintenance of the geometry of the cask's inventory is essential because the SNF rod cladding and the cladding of the vitrified highly active waste are stipulated as a barrier in the storage concept. For SNF, the cladding integrity is ensured currently by limiting the hoop stress and hoop strain as well as the maximum temperature to certain values for a 40-year storage period. For a prolonged storage period, other cladding degradation mechanisms such as inner and outer oxide layer formation, hydrogen pick up, irradiation damages in cladding material crystal structure, helium production from alpha decay, and long-term fission gas release may become leading effects driving degradation mechanisms that have to be discussed.
Jeong, Chang-Ho;Jeong, Hee-Rok;Choi, Sung-Gil;Heo, Ho Jin
Journal of agriculture & life science
/
v.46
no.2
/
pp.115-127
/
2012
Antioxidant and neuronal cell protective effects of aqueous extract from lotus (Nelumbo nucifera) leaf tea (LLTE) were investigated. The 2,2'-azino-bis (3-ethylbenzthiazoline-6-sulfonic acid) radical scavenging effect, ferric reducing antioxidant power, and malondialdehyde inhibition of LLTE were increased in a dose dependent manner. Intracellular reactive oxygen species accumulation resulting from hydrogen peroxide ($H_2O_2$) treatment was significantly reduced when LLTE were present in the media compared to PC12 cells treated with $H_2O_2$ only. In neuronal cell viability assay using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazoliumbromide (MTT), LLTE showed protective effect against $H_2O_2$-induced neurotoxicity. In addition, lactate dehydrogenase release into medium was also inhibited by LLTE (7.13-43.89%). Total phenolics of LLTE were 33.16 mg/g and a quercetin was identified as major phenolics (105.93 mg/100g). Therefore, above these data suggest that LLTE including quercetin may be useful in the natural antioxidant substance, and may reduce the risk of neurodegenerative disease.
Cheol Ho Park;Hyun Sook Lee;Man Sup Kwak;Jeon-Soo Shin
IMMUNE NETWORK
/
v.21
no.5
/
pp.36.1-36.16
/
2021
Peroxiredoxins (Prxs) are ubiquitously expressed peroxidases that reduce hydrogen peroxide or alkyl peroxide production in cells. Prxs are released from cells in response to various stress conditions, and they function as damage-associated molecular pattern molecules. However, the secretory mechanism of Prxs and their roles have not been elucidated. Thus, we aimed to determine whether inflammasome activation is a secretory mechanism of Prxs and subsequently identify the effect of the secreted Prxs on activation of the classical complement pathway. Using J774A.1, a murine macrophage cell line, we demonstrated that NLRP3 inflammasome activation induces Prx1, Prx2, Prx5, and Prx6 secretion in a caspase-1 dependent manner. Using HEK293T cells with a transfection system, we revealed that the release of Prx1 and Prx2 relies on gasdermin-D (GSDMD)-mediated secretion. Next, we confirmed the binding of both Prx1 and Prx2 to C1q; however, only Prx2 could induce the C1q-mediated classical complement pathway activation. Collectively, our results suggest that inflammasome activation is a secretory mechanism of Prxs and that GSDMD is a mediator of their secretion. Moreover, secreted Prx1 and Prx2 bind with C1q, but only Prx2 mediates the classical complement pathway activation.
Chang, Joon;Michael, John R.;Kim, Se-Kyu;Kim, Sung-Kyu;Lee, Won-Young;Kang, Kyung-Ho;Yoo, Se-Hwa;Chae, Yang-Seok
Tuberculosis and Respiratory Diseases
/
v.45
no.6
/
pp.1265-1276
/
1998
Background : Nitric oxide(NO) is an endogenously produced free radical that plays an important role in regulating vascular tone, inhibition of platelet aggregation and white blood cell adhesion to endothelial cells, and host defense against infection. The highly reactive nature of NO with oxygen radicals suggests that it may either promote or reduce oxidant-induced cell injury in several biological pathways. Oxidant injury and interactions between pulmonary vascular endothelium and leukocytes are important in the pathogenesis of acute lung injury, including acute respiratory distress syndrome(ARDS). In ARDS, therapeutic administration of NO is a clinical condition providing exogenous NO in oxidant-induced endothelial injury. The role of exogenous NO from NO donor or the suppression of endogenous NO production was evaluated in oxidant-induced endothelial injury. Method : The oxidant injury in cultured rat lung microvascular endothelial cells(RLMVC) was induced by hydrogen peroxide generated from glucose oxidase(GO). Cell injury was evaluated by $^{51}$chromium($^{51}Cr$) release technique. NO donor, such as S-nitroso-N-acetylpenicillamine(SNAP) or sodium nitroprusside(SNP), was added to the endothelial cells as a source of exogenous NO. Endogenous production of NO was suppressed with N-monomethyl-L-arginine(L-NMMA) which is an NO synthase inhibitor. L-NMMA was also used in increased endogenous NO production induced by combined stimulation with interferon-$\gamma$(INF-$\gamma$), tumor necrosis factor-$\alpha$(TNF-$\alpha$), and lipopolysaccharide(LPS). NO generation from NO donor or from the endothelial cells was evaluated by measuring nitrite concentration. Result : $^{51}Cr$ release was $8.7{\pm}0.5%$ in GO 5 mU/ml, $14.4{\pm}2.9%$ in GO 10 mU/ml, $32.3{\pm}2.9%$ in GO 15 mU/ml, $55.5{\pm}0.3%$ in GO 20 mU/ml and $67.8{\pm}0.9%$ in GO 30 mU/ml ; it was significantly increased in GO 15 mU/ml or higher concentrations when compared with $9.6{\pm}0.7%$ in control(p < 0.05; n=6). L-NMMA(0.5 mM) did not affect the $^{51}Cr$ release by GO. Nitrite concentration was increased to $3.9{\pm}0.3\;{\mu}M$ in culture media of RLMVC treated with INF-$\gamma$ (500 U/ml), TNF-$\alpha$(150 U/ml) and LPS($1\;{\mu}g/ml$) for 24 hours ; it was significantly suppressed by the addition of L-NMMA. The presence of L-NMMA did not affect $^{51}Cr$ release induced by GO in RLMVC pretreated with INF-$\gamma$, TNF-$\alpha$ and LPS. The increase of $^{51}Cr$ release with GO(20 mU/ml) was prevented completely by adding 100 ${\mu}M$ SNAP. But the add of SNP, potassium ferrocyanate or potassium ferricyanate did not protect the oxidant injury. Nitrite accumulation was $23{\pm}1.0\;{\mu}M$ from 100 ${\mu}M$ SNAP at 4 hours in phenol red free Hanks' balanced salt solution. But nitrite was not detectable from SNP upto 1 mM The presence of SNAP did not affect the time dependent generation of hydrogen peroxide by GO in phenol red free Hanks' balanced salt solution. Conclusion : Hydrogen peroxide generated by GO causes oxidant injury in RLMVC. Exogenous NO from NO donor prevents oxidant injury, and the protective effect may be related to the ability to release NO. These results suggest that the exogenous NO may be protective on oxidant injury to the endothelium.
The effect of antioxidants on the myocardial cellular damage which occurs during reoxygenation of hypoxic myocardium was examined in isolated rat hearts. The roles of oxygen free radical and lipid peroxidation in reoxygenation injury of myocardium were also investigated. In Langenorff preparation of isolated rat heart, which was made hypoxic by perfusion with the substrate free, hypoxic cardioplegic solution ($37^{\circ}C$, 90 min), the release of cytosolic enzymes (creatine phosphokinase, lactic dehydrogenase) and a lipid peroxidation product, malondialdehyde into the coronary effluent were abruptly increased by reoxygenation. The release of enzymes was closely parallel to that of MDA. These increases of enzymes and lipid peroxidation product were suppressed to various degrees in the presence of scavengers of superoxide anion (superoxide dismutase, 10,000 U), hydrogen peroxide (catalase, 25,000 U) and hydroxyl radical (dimethyl sulfoxide, 10%). A natural antioxidant, ${\alpha}-tocopherol$(4.5 uM) and a synthetic one, butylated hydroxytoluene (2 uM) suppressed the release of cytosolic enzymes with the concomittent reduction of lipid peroxidation as measured by malondialdehyde release into the coronary effluent. These effects of antioxidants were dose dependent, and were more pronounced when the antioxidants were administered throughout hypoxic and reoxygenation periods than given during reoxygenation period only. These results suggest that cytotoxic oxygen free radicals produced in the myocardium during reoxygenation may be responsible fur the myocardial cellular injury by enhancing the lipid peroxidation of cellular membranes. Furthermore, the antioxidants may exert protective effect against reoxygenation damage of hypoxic myocardium through the inhibition of lipid peroxidation reaction.
Oil shale is a sedimentary rock that contains organic compounds called kerogen that are released as petroleum-like liquids by retorting. In order to evalute oil shale as alternative oil resources, the physical properties of oil shale samples from US and Russia were investigated and Fischer assays were carried out. Thermogravimetric analysis shows that thermal degradation of oil shale consisted of two stage processes, with hydrocarbon release from kerogen followed by $CO_2$ release by carbonate decomposition. Organic compounds in oil shale have an high hydrogen/carbon ratio, and therefore liquid hydrocarbons could be obtained easily. Shale oil yields from Russian and US oil shales by Fischer assay were 12.7% and 18.5%, respectively. The density and boiling point of shale oils are higher than that of Middle East crude oil, indicating that further upgrading processes are necessary for refinery. On the other hands, sulfur contents are relatively low, and the amounts of Vanadium and Nickel are extremely small in shale oil. It was found that paraffins were rich in US shale oil while main components of Russian shale oil were oxygenated hydrocarbons.
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