• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.20 no.4
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• pp.259-262
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• 2017

Mitochondria play essential role in eukaryotic cells including in the oxidative phosphorylation and generation of adenosine triphosphate via the electron-transport chain. Therefore, defects in mitochondrial DNA (mtDNA) can result in mitochondrial dysfunction which leads to various mitochondrial disorders that may present with various neurologic and non-neurologic manifestations. Mutations in the nuclear gene polymerase gamma (POLG) are associated with mtDNA depletions, and Alpers-Huttenlocher syndrome is one of the most severe manifestations of POLG mutation characterized by the clinical triad of intractable seizures, psychomotor regression, and liver failure. The hepatic manifestation usually occurs late in the disease's course, but in some references, hepatitis was reportedly the first manifestation. Liver transplantation was considered contraindicated in Alpers-Huttenlocher syndrome due to its poor prognosis. We acknowledged a patient with the first manifestation of the disease being hepatic failure who eventually underwent liver transplantation, and whose neurological outcome improved after cocktail therapy.

• Journal of Microbiology and Biotechnology
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• v.30 no.12
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• pp.1876-1884
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• 2020

Ethanol often accumulates during the process of wine fermentation, and mitophagy has critical role in ethanol output. However, the relationship between mitophagy and ethanol stress is still unclear. In this study, the expression of ATG11 and ATG32 genes exposed to ethanol stress was accessed by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). The result indicated that ethanol stress induced expression of the ATG11 and ATG32 genes. The colony sizes and the alcohol yield of atg11 and atg32 were also smaller and lower than those of wild type strain under ethanol whereas the mortality of mutants is higher. Furthermore, compared with wild type, the membrane integrity and the mitochondrial membrane potential of atg11 and atg32 exhibited greater damage following ethanol stress. In addition, a greater proportion of mutant cells were arrested at the G1/G0 cell cycle. There was more aggregation of peroxide hydrogen (H2O2) and superoxide anion (O2•-) in mutants. These changes in H2O2 and O2•- in yeasts were altered by reductants or inhibitors of scavenging enzyme by means of regulating the expression of ATG11 and ATG32 genes. Inhibitors of the mitochondrial electron transport chain (mtETC) also increased production of H2O2 and O2•- by enhancing expression of the ATG11 and ATG32 genes. Further results showed that activator or inhibitor of autophagy also activated or inhibited mitophagy by altering production of H2O2 and O2•. Therefore, ethanol stress induces mitophagy which improves yeast the tolerance to ethanol and the level of mitophagy during ethanol stress is regulated by ROS derived from mtETC.

• Applied Biological Chemistry
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• v.30 no.4
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• pp.364-370
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• 1987

The $O_2^-$ level of the extract from young rice leaves, which was cold treated for 2 days and then placed at room temperature for a period of time significantly higher than that from tissues untreated. $O_2^-$ level in leaves was practically unchanged during cold treatment for 48 hours. But it started to increase to arrive at maximum in 8 hours, once the plants were placed under room temperature. The abnormal production of $O_2^-$ in mitochondria during postchilling process was interpreted as a biochemical consequence of accumulation of glycolysis product(s) in cytosol and/or NADH in mitochondrial matrix due to disruption of catabolic balance at low temperature. Mitochondria isolated from the chilling injured tissue was found to have lost considerably their respiratory activity. This fact may imply the involvement of intramitochondrial accumulation of $O_2^-$ in the inactivation of electron transport chain system. The observation that mitochondria in the presence of the $O_2^--producing$ enzymatic system (Xanthine/Xanthine oxidase) lost their respiratory activity supports this inference. It was also found in this work that Superoxide dismutase (SOD) is a substrate inducible enzyme, and that SOD is a possible protective agent in plant cell against chilling injury.

• KOREAN JOURNAL OF CROP SCIENCE
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• v.52 no.1
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• pp.69-80
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• 2007

Among the photoactive semiconductors such as $TiO_2,\;ZnO,\;Fe_2O_3,\;WO_3,\;and\;CdSe,\;TiO_2$ is the most widely used as photocatalyst in different media, because of its lack of toxicity and stability. In this study, the effects of titanium dioxide were investigated to obtain the information of physiological change in rice plant. Light-adapted Chlorophyll flourescence index decreased and relative electron transport rate of rice leaves was activated by titanium dioxide under $2,400\;{\mu}mol\;m^{-2}\;s^{-1}$ PAR (Photosynthetic active radiation). Relative electron transport rate of rice leaf treated with titanium dioxide 10 ppm was high in order of $2,400\;{\mu}mol\;m^{-2}\;s^{-1}\;PAR,\;2,200\;{\mu}mol\;m^{-2}\;s^{-1}\;PAR,\;450\;{\mu}mol\;m^{-2}\;s^{-1}\;PAR$ and titanium dioxide 10 ppm (45.1%), control (32.4%), diuron 10 ppm (15.3%) under $2,400\;{\mu}mol\;m^{-2}\;s^{-1}\;PAR$. Titanium dioxide increased photosynthesis of the rice leaf under $13.6\;KJ\;m^{-2}\;day^{-1}$ UV-B only. With titanium dioxide 20 ppm, reduced UV-B ($0.15\;KJ\;m^{-2}\;day^{-1}$) intensity changed the induction of proteins and twenty-five proteins were identified. Among them, seventy proteins were up-regulated, four proteins were down-regulated and four proteins were newly synthesized. Function of these proteins was related to photosynthesis (52%), carbohydrate metabolism (4%), stress/defense (8%), secondary metabolism (4%), energy/electron transport (4%), and miscellaneous (28%).

• Journal of the Korean Chemical Society
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• v.41 no.3
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• pp.144-149
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• 1997

Organic electroluminescence devices(ELD) were fabricated using by molecularly doped method with N,N'-diphenyl-N,N'-bis(3-methylphenyl)-1,1'-biphenyl-4,4'-diamine(TPD) as a hole transport agent, squarylium dye as an emitting agent, and side chain liquid crystalline polymer(MCH) as matrix for TPD. An indium-tin-oxide(ITO) coated glass and an Mg electrode were used as the hole and the electron injecting electrode, respectively. The highest stability of ELD was obtained by spin coating method using dichloroethane as a solvent at a polymer/TPD concentration of 0.005 wt%. For the EL cell with ITO/polymer-TPD/SQ dye/Mg structure, we achieved light red luminescence at a current of 102 mA/$cm^2$ with an applied voltage of 23 V.

• Korean Journal of Oriental Medicine
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• v.8 no.2 s.9
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• pp.95-107
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• 2002

Yukmijihwang-tang(YM) is a noted herbal prescription in Chinese and Korean traditional medicines, and it has been known to reinforce the vital essence and has been widely used for a variety of disease such as stroke, osteoporosis, anti-tumor, and hypothyrodism. Regarding its traditional use, YM has been known to reinforce the Yin (vital essence) of liver and kidney. Also it has been known to reinforce nutrition and biological function in brain. Recently, studies suggested that YM increase antioxidant activities and exert the protective effect against oxidant-induced liver cell injury. We investigated the high-throughput gene expression analysis on the Yukmijihwang-tang administrated in SD rats. Microarray data were validated on a limited number of genes by semiquantitative RT-PCR and Western blot analyses. The recent availability of microarrays provides an attractive strategy for elaborating an unbiased molecular profile of large number of genes in drug discovery This experimental approach offers the potential to identify molecules or cellular pathways not previously associated with herbal medicine. Total RNA from normal control brain and Yukmijihwang-tang administrated brain were hybridized to microarrays containing 10,000 rat genes. The 52 genes were found to be up-regulated(twice or more) excluding EST gene. The nine genes were found to be down-regulated(twice or more) excluding EST gene. Gene array technology was used to identify for the first time many genes expression pathway analysis that arecell cycle pathway, apoptosis pathway, electron transport chain pathway, cytoplasmic ribosomal protein pathway, fatty acid degradation pathway, and TGF-beta signaling pathway. These differentially expressed genes pathway analysis have not previously been iavestigated in the context of herbal medicine efficacy and represent novel factors for further study of the mechanism of herbal medicine efficacy.

• Journal of Physiology & Pathology in Korean Medicine
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• v.23 no.4
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• pp.888-894
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• 2009

It has been reported that silibinin, a natural polyphenolic flavonoid, induces cell death in various cancer cell types. However, the underlying mechanisms by which silibinin induces apoptosis in human glioma cells are poorly understood. The present study was therefore undertaken to examine the effect of silibinin on glioma cell apoptosis and to determine its underlying mechanism in human glioma cells. Apoptosis was estimated by FACS analysis. Reactive oxygen species (ROS) generation and mitochondrial membrane potential (${\Psi}m$) were measured using fluorescence dyes DCFH-DA and $DiOC_6$(3), respectively. Cytochrome c release from mitochondria and caspase-3 activation were estimated by Western blot analysis using specific antibodies. Exposure of cells to 30 mM silibinin induced apoptosis starting at 6 h, with increasing effects after 12-48h in a time-dependent manner. Silibinin caused ROS generation and disruption of ym, which were associated with the silibinin-induced apoptosis. The silibinin-induced ROS generation and disruption in ym were prevented by inhibitors of mitochondrial electron transport chain. The hydrogen peroxide scavenger catalase blocked ROS generation and apoptosis induced by silibinin. Silibinin induced cytochrome c release into cytosolic fraction and its effect was prevented by catalase and cyclosporine A. Silibinin treatment caused caspase-3 activation, which was inhibited by DVED-CHO and cyclosporine A. Pretreatment of caspase inhibitors also protected against the silibinin-induced apoptosis. These findings indicate that ROS generation plays a critical role in the initiation of the silibinin-induced apoptotic cascade by mediation of the mitochondrial apoptotic pathway including the disruption of ${\Psi}m$, cytochrome c release, and caspase-3 activation.

• Molecules and Cells
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• v.37 no.9
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• pp.672-684
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• 2014

The exact causes of cell death in Parkinson's disease (PD) remain unknown despite extensive studies on PD.The identification of signaling and metabolic pathways involved in PD might provide insight into the molecular mechanisms underlying PD. The neurotoxin 1-methyl-4-phenylpyridinium ($MPP^+$) induces cellular changes characteristic of PD, and $MPP^+$-based models have been extensively used for PD studies. In this study, pathways that were significantly perturbed in $MPP^+$-treated human neuroblastoma SH-EP cells were identified from genome-wide gene expression data for five time points (1.5, 3, 9, 12, and 24 h) after treatment. The mitogen-activated protein kinase (MAPK) signaling pathway and endoplasmic reticulum (ER) protein processing pathway showed significant perturbation at all time points. Perturbation of each of these pathways resulted in the common outcome of upregulation of DNA-damage-inducible transcript 3 (DDIT3). Genes involved in ER protein processing pathway included ubiquitin ligase complex genes and ER-associated degradation (ERAD)-related genes. Additionally, overexpression of DDIT3 might induce oxidative stress via glutathione depletion as a result of overexpression of CHAC1. This study suggests that upregulation of DDIT3 caused by perturbation of the MAPK signaling pathway and ER protein processing pathway might play a key role in $MPP^+$-induced neuronal cell death. Moreover, the toxicity signal of $MPP^+$ resulting from mitochondrial dysfunction through inhibition of complex I of the electron transport chain might feed back to the mitochondria via ER stress. This positive feedback could contribute to amplification of the death signal induced by $MPP^+$.

• Journal of Microbiology and Biotechnology
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• v.13 no.4
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• pp.544-551
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• 2003

Interactive effects of UV-B and Cd on growth, pigment, photosynthesis, and lipid peroxidation have been studied in Anabaena, Microcystis, and Nostoc; all the tested cyanobacteria showed differential sensitivity to different dosage of UV-B and Cd alone as well as in combination. Phycocyanin was severely affected by UV-B and Cd by all the strains; the degree of pigment bleaching was most pronounced in Anabaena followed by Microcystis and Nostoc. $UV-B_2+Cd_2$ produced nearly 83, 78, and 65% inhibition of phycocyanin in Anabaena, Microcystis, and Nostoc, respectively. The above treatment also significantly decreased the contents of Chl ${\alpha}$ and carotenoid. Presence of capsule in Microcystis protected the phycocyanin bleaching as compared to decapsulated cells. Laboratory-grown Microcystis revealed about 75 and 80% inhibition, following $UV-B_2+Cd_2$ treatment, respectively. in capsulated and decapsulated cells. Damage caused by Cd was more pronounced than UV-B. Inhibition of photosynthesis did occur in all the test strains, being maximum in Anabaena. PS II was the most sensitive component of the electron transport chain, showing 84, 80, and 70% inhibition in Anabaena, Microcystis, and Nostoc, respectively. As compared to control, significant lipid peroxidation (6.5-fold higher) was observed in Anabaena with $UV-B_2+Cd_2$, $^{14}C-uptake$ was more susceptible to Cd and Uv-B than oxygen-evolution. Approximately 84, 80, and 76% inhibition of $^{14}C-uptake$ was observed in Anabaena, Microcystis, and Nostoc, respectively. Similarly, $UV-B_2+Cd_2$ inhibited APT content of Anabaena by 87%. This ,study suggests that inhibition of carbon fixation was due to decreased ATP content of the test cyanobacteria by UV-B+Cd, where Anabaena was the most sensitive and Nostoc the most tolerant.

• Journal of Microbiology and Biotechnology
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• v.28 no.12
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• pp.1982-1991
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• 2018

Ethanol accumulation inhibited the growth of Saccharomyces cerevisiae during wine fermentation. Autophagy and the release of reactive oxygen species (ROS) were also induced under ethanol stress. However, the relation between autophagy and ethanol stress was still unclear. In this study, expression of the autophagy genes ATG1 and ATG8 and the production of ROS under ethanol treatment in yeast were measured. The results showed that ethanol stress very significantly induced expression of the ATG1 and ATG8 genes and the production of hydrogen peroxide ($H_2O_2$) and superoxide anion (${O_2}^{{\cdot}_-}$). Moreover, the atg1 and atg8 mutants aggregated more $H_2O_2$ and ${O_2}^{{\cdot}_-}$ than the wild-type yeast. In addition, inhibitors of the ROS scavenging enzyme induced expression of the ATG1 and ATG8 genes by increasing the levels of $H_2O_2$ and ${O_2}^{{\cdot}_-}$. In contrast, glutathione (GSH) and N-acetylcystine (NAC) decreased ATG1 and ATG8 expression by reducing $H_2O_2$ and ${O_2}^{{\cdot}_-}$ production. Rapamycin and 3-methyladenine also caused an obvious change in autophagy levels and simultaneously altered the release of $H_2O_2$ and ${O_2}^{{\cdot}_-}$. Finally, inhibitors of the mitochondrial electron transport chain (mtETC) increased the production of $H_2O_2$ and ${O_2}^{{\cdot}_-}$ and also promoted expression levels of the ATG1 and ATG8 genes. In conclusion, ethanol stress induced autophagy which was regulated by $H_2O_2$ and ${O_2}^{{\cdot}_-}$ derived from mtETC, and in turn, the autophagy contributed to the elimination $H_2O_2$ and ${O_2}^{{\cdot}_-}$.