• Title, Summary, Keyword: Mn-SOD

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Protective Effects of Antoxidant Enzymes of Candida albicans against Oxidative Killing by Macrophages

  • Kim, Hye-Jin;Na, Byoung-Kuk;Kim, Moon-Bo;Park, Duk-Young;Song, Chul-Yong
    • Journal of Microbiology
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    • v.37 no.2
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    • pp.117-122
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    • 1999
  • Protective roles of antioxidant enzymes, copper-zinc superoxide dismutase (CuZnSOD), manganese superoxide dismutase (MnSOD), and catalase of Candida albicans against exogenous reactive oxygens and oxidative killing by macrophages were investigated. The initial growth of C. albicans was inhibited by reactive, oxygen-producing chemicals such as hydrogen peroxide, pyrogallol, and paraquat, but it was restored as the production of antioxidant enzymes were increased. The growth inhibition of C. albicans by reactive, oxygen-producing chemicals was reduced by treating the purified candidal SOD and catalase. Also, in the presence of SOD and catalase, the oxidative killing of C. albicans by macrophages was significantly inhibited. These results suggest that antioxidant enzymes, CuZnSOD, MnSOD, and catalase of C. albicans may play important roles in the protection of C. albicans not only from exogenous oxidative stress but also from oxidative killing by macrophages.

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Anaerobic Respiration of Superoxide Dismutase-Deficient Saccharomyces cerevisiae under Oxidative Stress

  • Lee, Sun-Mi;Nam, Doo-Hyun
    • Biotechnology and Bioprocess Engineering:BBE
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    • v.3 no.1
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    • pp.15-18
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    • 1998
  • The entanol productivity of superoxide dismutase (SOD)-deficient mutants of Saccharo-Myces cerevisiae was examined under the oxidative stress by Paraquat. It was observed that MnSOD-deficient mutant of S. cerevisiae had higher ethanol productivity than wild type or CuZnSOD-deficient yeast both in aerobic and in anaerobic culture condition. Pyruvated dehydrogenase activity decreased by 35% and alcohol dehydrogenase activity increased by 32% were observed in MnSOD-deficient yeast grown aerobically. When generating oxygen radicals by Paraquat, the ehanol productivity was increased by 40% in CuZnSOD-deficient or wild strain, resulting from increased activity of alcohol dehydrogenase and decreased a activity of pyruvate dehydrogenase. However, the addition of ascorbic acid with Paraquat returned the enzyme activities at the level of control. These results imply that SOD-deficiency in yeast strains may cause the metabolic flux to shift into anaerobic ethanol fermentation in order to avoid their oxidative damages by Paraquat.

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Effect of Metal Ions on Speroxide Dismutase of the Liver in Senescence-Accelerated Mouse(SAM) (노화촉진생쥐(SAM)의 간에서 금속이온이 SOD의 활성에 미치는 영향)

  • 양미경;박문숙
    • Journal of environmental and Sanitary engineering
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    • v.15 no.2
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    • pp.1-9
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    • 2000
  • This research employed a senescence-accelerated mouse(SAM) to explore the possibility that differences exits among the major antioxidants, superoxid dismutase(SOD), in terms of ability to protect such animal treated with Cu, Fe and Mn. To assess the antioxidants function of metal ions on SAM-R/1 and SAM-P/8 were administered with Cu, Fe and Mn orally. The effect of metal ions on SAM towards reversing oxygen sensitivity was determined as a bioassays of SOD in the mouse liver. The data show that the SOD activity was induced by each metal ions in both SAM-R/1 and SAM-P/8. It suggested that induced SOD by each metal ions may protect against oxidative mediated stress. Finally, overall data lead to the possibility of metal ions as an antioxidants or each metal ions act producer of oxygen radicals in the liver of SAM-R/1 and SAM-P/8.

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Mechanism for Antioxidant Activity of Nardostachys chinensis root Extract

  • Heo, Jee-In;Kim, Jeong-Hyeon;Lee, Jeong-Min;Kim, Sung Chan;Park, Jae-Bong;Kim, Jaebong;Lee, Jae-Yong
    • Journal of Applied Biological Chemistry
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    • v.57 no.1
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    • pp.17-22
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    • 2014
  • Nardostachys chinensis (N. chinensis) has been used in traditional medicine as a sedative and analgesic. It has been reported that N. chinensis extract has an antioxidant activity. However, the mechanism has not been elucidated. In this study, we showed that FOXO3a was activated by N. chinensis extract. FOXO3a is a transcriptional factor that involved in cell cycle arrest, DNA repair, apoptosis, and detoxification of reactive oxygen spices (ROS). Protein level of FOXO3a was increased by N. chinensis extract whereas phospho-FOXO3a (Thr 32) was not changed. Promoter activities of target genes of FOXO3a such as MnSOD, p27, and GADD45 were increased by N. chinensis extract. Among target genes, protein level of MnSOD was increased by N. chinensis extract, and this leads to removal of ROS level in human embryonic fibroblast (HEF) cells. These results suggested that N. chinensis extract has an antioxidant activity by upregulation of MnSOD through FOXO3a activation.

Protein kinase C beta II upregulates intercellular adhesion molecule-1 via mitochondrial activation in cultured endothelial cells

  • Joo, Hee Kyoung;Lee, Yu Ran;Choi, Sunga;Park, Myoung Soo;Kang, Gun;Kim, Cuk-Seong;Jeon, Byeong Hwa
    • The Korean Journal of Physiology and Pharmacology
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    • v.21 no.4
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    • pp.377-384
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    • 2017
  • Activation of protein kinase C (PKC) is closely linked with endothelial dysfunction. However, the effect of $PKC{\beta}II$ on endothelial dysfunction has not been characterized in cultured endothelial cells. Here, using adenoviral $PKC{\beta}II$ gene transfer and pharmacological inhibitors, the role of $PKC{\beta}II$ on endothelial dysfucntion was investigated in cultured endothelial cells. Phorbol 12-myristate 13-acetate (PMA) increased reactive oxygen species (ROS), p66shc phosphorylation, intracellular adhesion molecule-1, and monocyte adhesion, which were inhibited by $PKC{\beta}i$ (10 nM), a selective inhibitor of $PKC{\beta}II$. PMA increased the phosphorylation of CREB and manganese superoxide dismutase (MnSOD), which were also inhibited by $PKC{\beta}i$. Gene silencing of CREB inhibited PMA-induced MnSOD expression, suggesting that CREB plays a key role in MnSOD expression. Gene silencing of $PKC{\beta}II$ inhibited PMA-induced mitochondrial ROS, MnSOD, and ICAM-1 expression. In contrast, overexpression of $PKC{\beta}II$ using adenoviral $PKC{\beta}II$ increased mitochondrial ROS, MnSOD, ICAM-1, and p66shc phosphorylation in cultured endothelial cells. Finally, $PKC{\beta}II$-induced ICAM-1 expression was inhibited by Mito-TEMPO, a mitochondrial ROS scavenger, suggesting the involvement of mitochondrial ROS in PKC-induced vascular inflammation. Taken together, the results suggest that $PKC{\beta}II$ plays an important role in PMA-induced endothelial dysfunction, and that the inhibition of $PKC{\beta}II$-dependent p66shc signaling acts as a therapeutic target for vascular inflammatory diseases.

Responses of Transgenic Tobacco Plants Overexpressing Superoxide Dismutase and Ascorbate Peroxidase in Chloroplasts to Water Stress (Superoxide Dismutase와 Ascorbate Peroxidase를 엽록체에 과발현하는 형질전환 담배의 수분스트레스에 대한 반응)

  • 최선미;권석윤;곽상수;박용목
    • Journal of Environmental Science International
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    • v.10 no.1
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    • pp.79-84
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    • 2001
  • To assess resistance of transgenic tobacco plants which overexpress superoxide dismutase (SOD) and ascorbate peroxidase (APX) in chloroplasts to water stress, changes in leaf water potential, turgor potential, stomatal conductance and transpiration rate were measured. Leaf water potential in all plants remained high up to day 4 after withholding water but thereafter decreased markedly. In spite of a remarkable decrease in leaf water potential, some of transgenic plants maintained higher turgor potential compared with control plant on day 12. In particular, the transgenic plant expressing MnSOD showed an outstanding maintenance in turgor pressure by osmotic adjustment throughout the experiment, resulting in high stomatal conductance and transpiration rate. However, among transgenic plants, osmotic potential was reduced more effectively in multiple transformants such as the double transformant expressing both MnSOD and APX, and the triple transformant expressing CuznSOD, MnSOD and APX than single transformants. Consequently, further research is needed to get general agreement on the tolerance of transgenic plants to water stress at different growth stages for each transgenic plant.

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Effect of Treadmill Exercise Training on the Expression of PGC-1α, GLUT-1, Tfam Proteins and Antioxydent Ezymes in Brain of STZ-Induced Diabetic Rats (트레드밀 지구성 운동이 streptozotocin으로 유발된 당뇨 흰쥐의 뇌에서 PGC-1α, GLUT-1, Tfam 단백질 및 항산화 효소(Cu, Zn-SOD, Mn-SOD)의 발현량에 미치는 영향)

  • Park, Noh-Hwan;Lee, Jin;Jung, Kook-Hyun;Choi, Bong-Am;Jang, Hyung-Chae;Lee, Suk-In;Lee, Dong-Soo;Cho, Joon-Yong
    • Journal of Life Science
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    • v.21 no.3
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    • pp.435-443
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    • 2011
  • The purpose of this study is to identify the effects of exercise training [ET, 10~18 m/min (speed), 20~30 min (exercise duration)/a day for 5 day/wk, 6 wk) on PGC-$1{\alpha}$, GLUT-1, Tfam, Cu,Zn-SOD and Mn-SOD proteins in brain of STZ-induced diabetic rats. The male Sprague-Dawley (SD) rats were single-injected intraperitoneally with 50mg/kg of streptozotocin (STZ) to produce STZ-induced diabetic rats. Rats were divided into 3 experimental groups with 8 rats in each group, as follows: (1) non-STZ group (n=8), (2) STZ-CON group (n=8), (3) STZ-EXE group (n=8). The results of this study suggest that i) serum glucose level was significantly reduced in STZ-EXE group compared with STZ-CON group (p<0.05), ii) PGC-$1{\alpha}$ (p<0.001), mtPGC-$1{\alpha}$ (p<0.001), GLUT-1 (p<0.001), and mtTfam (p<0.001) proteins in brain of STZ-induced diabetic rats were significantly increased in STZ-EXE group compared with STZ-CON group, iii) Cu,Zn-SOD (p<0.001) and Mn-SOD (p<0.01) proteins in the STZ-induced diabetic rats were significantly increased in STZ-EXE group compared with STZ-CON group. In conclusion, the findings of the present study reveal that treadmill exercise training increases brain GLUT-1 protein level possibly through up-regulation of PGC-$1{\alpha}$ and Tfam proteins which represent key regulatory components of stimulation of brain mitochondrial biogenesis. In addition, treadmill exercise training may prevent oxidative stress by up-regulation of Cu,Zn-SOD and Mn-SOD proteins in the STZ-induced diabetic rats.

An Efficient Method for the Expression and Reconstitution of Thermostable Mn/Fe Superoxide Dismutase from Aeropyrum pernix K1

  • Lee, Hee-Jin;Kwon, Hye-Won;Koh, Jong-Uk;Lee, Dong-Kuk;Moon, Ja-Young;Kong, Kwang-Hoon
    • Journal of Microbiology and Biotechnology
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    • v.20 no.4
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    • pp.727-731
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    • 2010
  • The gene APE0743 encoding the superoxide dismutase (ApSOD) of a hyperthermophilic archaeon Aeropyrum pernix K1 was cloned and overexpressed as a GST fusion protein at a high level in Escherichia coli. The expressed protein was simply purified by the process of glutathione affinity chromatography and thrombin treatment. The ApSOD was a homodimer of 25 kDa subunits and a cambialistic SOD, which was active with either Fe(II) or Mn(II) as a cofactor. The ApSOD was highly stable against high temperature. This thermostable ApSOD is expected to be applicable as a useful biocatalyst for medicine and bioindustrial processes.

Isolation and Characterization of the sod2$^{2+}$ Gene Encoding a Putative Mitochondrial Manganese Superoxide Dismutase in Schizosaccharomyces bombe

  • Jeong, Jae-Hoon;Kwon, Eun-Soo;Roe, Jung-Hye
    • Journal of Microbiology
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    • v.39 no.1
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    • pp.37-41
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    • 2001
  • The fission yeast Schizosaccharomyces pombe contains two distinct superoxide dismutase (SOD) activities, one in the cytosol encoded by the $sod2^{+}$ gene and the other in mitochondria. The $sod2^{+}$ gene encoding putative mitochondrial manganese superoxide dismutase (MnSOD) was isolated from the S. pombe genomic library using a PCR fragment as the probe. The nucleotide sequence of the $sod2^{+}$ gene and its flanking region (4051 bp HindIII fragment) was determined. An intron of 123 nt in size was predicted and confirmed by sequencing the cDNA following reverse transcription PCR. The predicted Sod2p consists of 218 amino acid residues with a molecular mass of 24,346 Da. The deduced amino acid sequence showed a high degree of homology with other MnSODs, especially in the metal binding residues at the active site and their relative positions. The transcriptional start site was mapped by primer extension at 231 at upstream from the ATG codon. A putative TATA box(TATAAAA) was located 58 nt upstream from the transcriptional start site and putative polyadenylation sites were located at 1000, 1062, and 1074 nt downstream from the ATG start codon.

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Effects of ischemic preconditioning, KATP channel on the SOD activation and apoptosis in ischemic reperfused skeletal muscle of rat (허혈양상화와 KATP 통로가 허혈후 재관류된 흰쥐의 골격근육에서 SOD 활성 및 apoptosis에 미치는 영향)

  • Abn, Dong-choon;Paik, Doo-jin;Yang, Hong-hyun
    • Korean Journal of Veterinary Research
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    • v.39 no.5
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    • pp.878-895
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    • 1999
  • Ischemic preconditioing (IPC), i.e., a preliminary brief episode of ischemia and reperfusion, has been shown to reduce the cell damage induced by long ischemia and reperfusion. Superoxide radical which is produced during reperfusion after ischemia was recognized as a factor of the ischemic injury and it is dismutated into $H_2O_2$ and $O_2$ by two types of intracellular superoxide dismutase (SOD), Cu,Zn-SOD in cytoplasm and Mn-SOD in mitochondria. Recently oxygen free radicals are suggested to induce the apoptosis, however mechanism of the reduced apoptosis by ischemic preconditioing was unknown, while many studies performed in mammalian heart indicated that ATP-sensitive $K^+$ ($K_{APT}$) channel activation related with the protective effects. The aim of present study is to investigate 1) whether IP upregulate the Cu,Zn-SOD and Mn-SOD activities, and 2) whether ischemic preconditioning decreases apoptosis via $K_{APT}$ channel activation in timely reperfused skeletal muscle after long ishemia. The experimental animals, Sprague-Dawley rats weighing 250~300g, were divided into 8 groups; 1) control group, 2) ischemic preconditioning only groups, 3) pinacidil, a $K_{APT}$ channel opener, treatment only groups, 4) glibenclamide, a $K_{APT}$ channel blocker, treatment only groups, 5) ischemia groups, 6) ischemia after IPC groups, 7) ischemia and pinacidil treatment groups, and 8) IP and ischemia after glibenclamide pretreatment groups. Animals of the control group were administered with the vehicle (DMSO) alone. Pinacidil (1mg/kg) was administered intravenously 5 minutes after initiation of ischemia, and glibenclamide (0.5mg/kg) was injected intravenously 20 minutes before IPC. In rats that were ischemic preconditioned, the left common iliac artery was occluded for 5 minutes followed by 5 minutes of reperfusion by three times using vascular clamp. Ischemia was done by occlusion of the same artery for 4 hours. The specimens of left rectus femoris muscle were obtained immediately (0 hour), 12 hours, 24 hours after drug administrations, IP or ischemia and reperfusion. The immunoreactivities of SOD and its alterations were observed by use of sheep antihuman Cu,Zn-SOD and Mn-SOD antibodies on the $10{\mu}m$ cryosections. The incidencies of apoptosis were observed by TUNEL methods with in situ apoptosis detection kit on $6{\mu}m$ paraffine section. The results obtained were as follows : 1. After IPC, immunoreactivities of Cu,Zn-SOD mainly in the small-sized fibers were increased by 24 hours, that of Mn-SOD at 0 hour and 24 hours. 2. No significant changes in immunoreactivities of SOD was observed in the pinacidil and in the glibenclamide treatment only groups, and in the ischemia only groups. 3. The immunoreactivities of the Cu,Zn-SOD were increased in the ischemia after IPC groups and the ischemia and pinacidil treatment groups. 4. The immunoreactivities of the Cu,Zn-SOD in the IPC and ischemia after glibenclamide pretreatment groups were not increased except for the 12 hours reperfusion group. But, Mn-SOD immunoreactivities were increased in the 0 hours, 12 hours and 24 hours after reperfusion. 5. In the control group, the IPC only groups, and the pinacidil treatment only groups, negative or trace apoptotic reactions were observed, but the positive apoptotic reaction occured in the glibenclamide treatment groups. 6. Moderate or many number of apoptosis were revealed in the ischemia groups, and also the IPC and ischemia after glibenclamide pretreatment group except for 12 hours and 24 hours after reperfusion. However, the incidence of apoptosis was decreased in the ischemia after IPC groups and in the ischemia and pinacidil treatment groups. 7. There is a coincidence between the increase of Cu,Zn-SOD immunoreactivities and the decrease of apoptosis in the presence of ischemia and reperfusion. These results suggest that the protective effects of ishemic preconditioing may related to the SOD activation, and the ischemic preconditioning decreases the apoptosis partially via $K_{APT}$ channel activation in timely reperfused rat skeletal muscle. It is also suggested that inhibition of apoptosis by IPC may related with the SOD activation.

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