• Title/Summary/Keyword: 산화제 결핍

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OH, PAHs and Soot Ditribution in a Laminar Diffusion Flame Under Oxidizer Deficient Ambience (산화제 결핍 분위기에서의 층류 확산화염내 OH, PAHs 및 그을음 분포)

  • Shim, Sung-Hoon;Shin, Hyun-Dong
    • Transactions of the Korean Society of Mechanical Engineers B
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    • v.26 no.10
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    • pp.1348-1354
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    • 2002
  • We investigate the flame behavior and spatial distribution of OH, PAHs and soot in a confined buoyant diffusion flame with decrease of the coflowing air flow rate. Direct photographs and Schlieren images represent that flame is Ally occupied by blue flame and becomes unstable, which is partially detached to the fuel nozzle tip in a near extinction flame under extremely reduced oxidizer condition. Laser induced fluorescence profiles clearly shows that OH is still generated in near-extinction flame, although intensity becomes weak with decreasing air flow rate. But soot scattering image cannot be seen any more in an oxidizer deficient ambience and simultaneously the PAHs are widely distributed downstream. These results are due to that a decrease of oxygen concentration in the combustion chamber leads to a temperature drop of flame, as a consequence, to a delay in soot growth and to a expanding of the PAHs, as soot precursors.

Effect of Neurogranin Phosphorylation on Oxidative Stress by Hydrogen Peroxide in Early Onset of Batten Disease (과산화수소에 의한 산화스트레스가 영아형 바텐병에서 neurogranin의 인산화에 미치는 영향)

  • Yoon, Dong-Ho;Kim, Han-Bok;Park, Joo-Hoon;Kim, Sung-Jo
    • Journal of Life Science
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    • v.19 no.4
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    • pp.520-525
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    • 2009
  • Early onset of Batten disease (EBD), one of the most lethal neurodegenerative storage disorders of childhood, is caused by inactivating mutations in the Ceroid Lipofuscinosis, Neuronal (CLN1) gene. Neurogranin, a calmodulin-binding protein, is expressed in the brain and participates in the protein kinase C (PKC) signaling pathway. While oxidative stress is the suggested cause of neurodegeneration in EBD, its molecular mechanism(s) remains obscure. In this research, we examined the levels of neurogranin in the brain mRNA of wild-type (WT) mice and EBD knockout (KO) mice, as well as the proteins. We also performed neuronal cultures to measure the expression levels of neurgranin and phosphorylated-neurogranin with or without oxidative stress inducers and anti-oxidants. Results showed that neurogranin in both EBD KO mice brain mRNA and protein extracts decreased in an age dependent manner. However, high amounts of phosphorylated-neurogranin were detected in the 6-month brain. This pattern was also confirmed by cultured neurospheres samples. Moreover, neurospheres treated with $H_2O_2$, an oxidative stress inducer, showed increased phosphorylated-neurogranin patterns. Interestingly, this pattern returned to normal status when treated with N-acetyl-L-cystein, an anti-oxidant, after $H_2O_2$ treatment was performed. Our results suggest that the phosphorylation of neurogranin is affected by oxidative stress status in EBD, and appropriate anti-oxidant treatment will relieve hyper-phosphorylation of neurogranin.

9-Methyl Folate, an Antagonist of Folic Acid : Ist Effect on the Metabolism of Folic Acid in the Rat (염산의 항비타민제인 9-Methyl Folate가 흰쥐의 엽산대사에 미치는 영향)

  • Min, Hye-Seon
    • Journal of Nutrition and Health
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    • v.24 no.4
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    • pp.337-343
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    • 1991
  • The effect of 9-methyl folate on histidine oxidation, the uptake of an injected dose of $[^{3}H]folate$ by the livers and kidneys, the hepatic and blood folate levels were investigated by feeding crude x-methyl folate(XMF) at a level of 5 g per kg diet. 9-Methyl folate is konwn as a major forate antagonist in XMF to produce deficiency signs in rat. Feeding of XMF decreased histidine oxidation and hepatic folate levels significantly, which showed the function of 9-methyl folate as an antifolate in rats. The hepatic uptake of labeled folate in XMF- fed rats was decreased significantly. These data led to conclude that 9-methyl folate inhibited folate uptake and retention by tissue, especially liver, which could explain the low liver folate levels and the decreased histidine oxidation. However, only very low level of 9-methyl folate was detected in liver. It suggested that 9-methyl folate may be metabolized very quickly in the liver after uptaken.

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Comparison of Morphology of Deposits on SiC Filaments with LIF Image in Propane/Air Laminar Diffusion Flames in an Oxidizer Deficient Environment (산화제 결핍 상태의 프로판 층류 확산화염에서 LIF 이미지와 SiC 필라멘트 부착물의 형태 비교)

  • Shim, Sung-Hoon;Yoo, Chang-Jong;Shin, Hyun-Dong
    • Journal of the Korean Society of Combustion
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    • v.7 no.4
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    • pp.1-9
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    • 2002
  • The morphology of deposits on $15-{\mu}m$ thin SiC filaments has been investigated with SEM and compared with UV-excited laser induced broadband fluorescences in co-flowing, propane laminar diffusion flames in a reduced oxidizer environment. The homogeneous morphology of droplet-like deposits inner flame zone and the agglomeration of condensed-phase deposits and the transition to soots from grown up droplet-like precursors with approaching the flame surface can be observed in a barely sooting flame. The average size of the mature soots deposited in the luminous flame edge is scarcely dependent on their axial position in a confined flame under reduced oxidizer condition. A double structure of PAH fluorescence is observed in near-extinction flames with further decreasing of oxidizer. A comparison of the PAH fluorescence with the morphologies of deposits indicates that appearance of the "dark" hollow zone is caused by a decreased number density of developed liquid-phase large molecules and the outer weak fluorescence zone is caused by the diffusion of gas-phase small molecules.

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The Measurement of Folacin Coutent in Korean Foods -Part I . Folate Distribution in Vegetables- (한국 상용 식품의 엽산 분석에 관한 연구 -제 I 보 채소류의 엽산치 분석-)

  • Kim, Young-Min
    • Journal of Nutrition and Health
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    • v.10 no.4
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    • pp.84-91
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    • 1977
  • 엽산의 결핍은 대혈구성 빈혈(macrocytic and/or megaloblastic anemia)을 일으킨다. 체내에서 엽산은 합성될 수 없는 것으로 알려져, 식품을 통하여 섭취하여야 한다. 이에, 한국인 식생활의 기본을 이루고 있는 쌀, 콩 및 채소류의 식품에 포함된 엽산치를 미생물학적인 측정방법에 따라 분석하였다. Streptococcus faecalis보다 Lactobacillus casei미생물을 사용하여 측정한 방법이, 인간에게 이용될 수 있는 보다 정확한 엽산치로 밝혀졌다. 산화되기 쉬운 형태로 된 labile folate를 보호하기 위한 ascorbic acid의 첨가는, 각 식품에 포함된 엽산치를 증가 시켰다. 결합형으로 존재하는 polyglutamates를 유리형으로 하기 위하여 conjugase enzyme을 사용하였으며, 식품에 따른 화학적 조성은 주로 polyglutamyl form이나 각 식품에 따라 큰 차이가 있는 것으로 나타났다. Lactobacillus casei을 사용하여 측정된 각 식품의 엽산치는, 배추 34.5, 당근17.8, 오이 25.3, 가지 24.7, 쑥갓 76.5, 마늘 3.1, 파 40.2, 완두콩 68.7, 풋고추 27.1, 강남콩 66.9, 부추 64.1, 상치 39.3, 양파 4.3, 시금치 150.7, 호박 26.1, 무우 40.3, 백미 29.9 ug으로 각기 식품 100g 중에 함유됨을 보였다.

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Effect of Dietary Supplementation of Vitamin A and Chronic Consumption of Ethanol on Oxidative Damage and Antioxidant System in Rats (비타민 A 보충 식이 및 에탄올의 만성적 급여가 흰쥐의 체내 산화적 손상과 항산화체계에 미치는 영향)

  • 양경미
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.32 no.2
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    • pp.278-286
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    • 2003
  • Alcohol is well known agent which can damage the human tissues such as liver via stimulating lipid peroxidation. On the other hand, carotenoids in addition to vitamins A, C and I play important roles in protecting these oxidative damages as well as preventing the production of free radicals. This study was carried out to investigate the effect of dietary vitamin A on lipid peroxidation and antioxidants status in ethanol-treated rats. In the experiment, male Sprague-Dawley rats weighing 160~180 g were given a liquid diet containing 36% of total calories as ethanol for 7 weeks. The pair-fed control rats received an isocaloric amount of diet containing sucrose instead of ethanol on the following day Additionally, the liquid diet contained adequate amount of $\beta$-carotene, retinyl acetate or 13-sis-reinoic acid except vitamin A-deficient diet. The results obtained are as follows. The levels of plasma and hepatic lipid peroxide were increased after chronic ethanol feeding in rats. Retinyl acetate supplementation significantly reduced lipid peroxidation induced by ethanol feeding Glucose 6-phosphatase activity was significantly reduced in rats fed vitamin A-deficient diet with ethanol and alkaline phosphatase activity was significantly induced in rats fed 13-cis-reinoic acid diet with ethanol. Catalase and alcohol dehydrogenase activities did not show a consistent tendency in experiment groups. The hepatic antioxidant enzyme activities did not significantly changed by chronic ethanol feeding groups. The striking decrease in conversion of $\beta$-carotene to retinol was observed in rats fed a $\beta$-carotene diet with ethanol feeding The level of retinol and retinoic acid in plasma and liver was decreased after chronic ethanol administration Based on this result, these data suggest that ethanol feeding enhances oxidative stress especially in those fed a vitamin A-deficient diet, and vitamin A supplementation, especially, retinyl acetate intake can prevent enhanced lipid peroxidation and related damage to some extent.

Effect of Calcium Compounds from Oyster Shell Bouind Fish Skin Gelatin Peptide in Calcium Deficient Rats (어피 젤라틴 펩티드와 결합한 굴껍질 유래 칼슘 화합물이 칼슘 결핍 흰쥐에 미치는 영향)

  • KIM Gyu-Hyung;JEON You-Jin;BYUN Hee-Guk;LEE Yeon-Sook;LEE Eung-Ho;KIM Se-Kwon
    • Korean Journal of Fisheries and Aquatic Sciences
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    • v.31 no.2
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    • pp.149-159
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    • 1998
  • To utilize the oyster shell containing a lot of calcium, we investigated the bioavailability of calcium compounds from oyster shell. First, calcium oxide was prepared by burning of oyster shell at $1200^{\circ}C$. Its purity was approximately $98.5\%$. Calcium compounds, $CaCl_2$, and $CaHPO_4$, from the calcium oxide were prepared by chemical reaction. Effect on calcium absorption by the calcium compounds from oyster shell was improved using fish skin gelatin peptides.(FSGP), which was prepared by enzymatic hydrolysis of fish skin gelatin for 4hr with tuna pyloric caeca crude enzyme (TPCCE). in vitro experiment, calcium absorption by addition of FSGP in a mixture solution of calcium and phosphate was higher approximately $70\%$ than that by control. in vivo using calcium deficient rats, a group taken the diets with $3\%$ FSGP and $CaHPO_4$ was significantly improved amount of calcium and ash in femur and strength of femur. These results suggest that calcium compounds from oyster shell and FSGP could be used as an effective dietary calcium source.

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Oxidative Stress and HSP70 Expression Upon Cerebral Isehemia-Reperfusion in Mongolian Gerbil (모래쥐에서 뇌의 허혈/재관류에 의한 산화성 스트레스 형성과 HSP70의 발현)

  • Park, Young-Mee;Kim, Chul-Hoon;Do, Yun-Jeong;Choi, Eun-Mi;Ahn, Young-Soo
    • The Korean Journal of Pharmacology
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    • v.32 no.3
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    • pp.335-345
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    • 1996
  • A critical role of oxygen-derived free radicals has been implicated in ischemia/reperfusion (I/R)-induced brain damage. In this study, we have produced experimental I/R to the brains of Mongolian gerbil (Meriones unguiculatus) by a transient occlusion and release of the common carotid arteries. We have attempted to determine whether the oxidative stress is generated upon I/R and whether this oxidative stress is linked to the cell damage. Since hippocampus has been suggested as one of the most vulnerable regions of the brain to the oxidative stress, we analyzed samples from hippocampus in comparison with those from cortex. In addition, we have examined the expression of heat shock protein 70kD species (HSP70) in these regions in order to evaluate a possible role of this protein in I/R-induced brain damage. To determine whether the oxidative stress is produced upon I/R, we measured the glutathione oxidation, GSSG/ (GSH + 2xGSSG), as an index of oxidative stress. We found an increase of the glutathione oxidation primarily in hippocampus upon I/R. To determine whether this oxidative stress is linked to the cell damage, we measured the degree of lipid peroxidation upon I/R. We found an increase of lipid peroxidation in both regions. However, the magnitude of increases was greater in hippocampus than in cortex. In addition, we found that changes in both the magnitude and the temporal patterns of glutathione oxidation closely correlated with those of lipid peroxidation. Our study provides biochemical evidences that the oxidative stress is generated upon I/R and this oxidative stress is linked to the oxidative cell damage. Our study also provides evidences that the degree of oxidative stress as well as oxidative cell damage is greater in hippocampus than in cortex. We could not find difference in the basal level of HSP70 expression between hippocampus and cortex, indicating that the intrinsic vulnerability of hippocampus cannot be explained by the lower level of HSP70 expression. We did find, however, that the induction of HSP70 expression upon I/R was impaired in the hippocampus. This impairment appeared to be at the transcriptional level. These results suggest that the measurement of HSP70 induction may be employed as a useful predictor of differential cellular susceptibilities to the I/R-induced brain damage.

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Effect of Additives on Paper Aging (종이 첨가제가 종이의 노화에 미치는 영향)

  • 윤병호;이명구;최경화
    • Journal of Korea Foresty Energy
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    • v.21 no.2
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    • pp.25-33
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    • 2002
  • One of the critical problems to preserve books and documents in libraries and archives is the deterioration. Some of previous results showed that the major cause of paper deterioration was the acid-catalyzed hydrolysis of the cellulose in paper fibres and aging rate of acidic paper was faster than that of alkaline paper. Therefore, It is necessary to remove the acid in the paper for reducing the rate of paper deterioration. It has been reported to extend the useful life of acidic paper by three to five times. Recently, It has been recognized the need for an effective method of deacidifying large quantities of books and document. However, in the previous many reports little attention was paid to the effect of paper additives. In this paper, We carried out experiment about the effect of additives on paper aging and the effect of deacidification by the gaseous ethanolamines (monoehtanolamine, diethanolamine, triehtanolamine). In result, it was found that the strength of aging was in the order of the alum+rosin>alum >AKD> control and the rate of deacidification was in the order of the monoethanolamine>diethanolamine>triethanolamine. The treatment with the gaseous ethanolamines caused decreasing of brightness and dropping of fold endurances. However, deacidification by combination treatment of the various gaseous ehtnaolamines prevented from decreasing of brightness and dropping of folding endurances.

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2020 Dietary Reference Intakes for Koreans: riboflavin (2020 한국인 영양소 섭취기준: 리보플라빈)

  • Lee, Jung Eun;Cho, Jin Ah;Kim, Ki Nam
    • Journal of Nutrition and Health
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    • v.55 no.3
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    • pp.321-329
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    • 2022
  • Riboflavin and its derivatives, flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD), are key components of mitochondrial energy metabolism and oxidation-reduction reactions. Proposed dietary reference intakes for Koreans (KDRIs), that is, estimated average requirements (EARs), for riboflavin, based on current knowledge of riboflavin and riboflavin derivative levels, and glutathione reductase activity, are 1.3 mg/d for men aged 19-64 years and 1.0 mg/d for women aged 19-64 years. By applying a coefficient of variance of 10%, reference nutrient intakes (RNIs) were set at 1.5 mg/d for men aged 19-64 years and 1.2 mg/d for women aged 19-64 years. Likewise, EARs and RNIs of riboflavin intake were proposed for all age groups and women in specific life stages such as pregnancy. Mean adult riboflavin intake for adults aged ≥ 19 years was 1.69 mg/d in Korea National Health and Nutrition Examination Survey (KNHANES) 2020, which was 124.9% of EAR according to the 2020 KDRIs. In the 2015-2017 KNHANES study, the mean riboflavin intake from foods and supplements was 2.79 mg/d for all age groups, and 32.7% of individuals consumed less riboflavin than EAR according to the 2020 KDRIs. For those that used supplements, mean intakes were 1.50 mg/d for riboflavin from foods, 10.26 mg/d from supplements, and 11.76 mg/d from food and supplements, and 5.5% of individuals consumed less riboflavin than EAR. Although the upper limit of riboflavin has not been established, the merits of increasing supplement use warrant further consideration. Also, additional epidemiologic and intervention studies are required to explore the role of riboflavin in the etiology of chronic diseases.