• Journal of Ginseng Research
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• 제14권2호
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• pp.310-316
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• 1990

This study was focused on the characterization of mitochondrial DNA (mtDNA) for molecular 9enetical approach of energy Production related mechanism in Panax ginseng. The simple and efficient method of mtDNA isolation from ginseng has been developed by modification of recently advanced methods. This procedure can successfully apply to mtDNA isolation of several plants. mtDNA of etiolated shoot and one-year root were digested with restriction endonucleases, but that of 6-year root not. Any difference was not observed in the restriction endonuclease digestion patterns among the ginseng variants. Molecular size of ginseng mtDNA was estimated at least 159 kb by the restriction endonuclease fragment analysis. The 4.5 kb extra band at the lane of EcoRII treatment could be observed in restriction patterns digested with the methylation sensitive endonucleases, BstN I and EcoRII. For construction of mitochondrial genomic library of ginseng, mtDNA was partially digested with EcoRl, and packaged with EMBL4 phage vector. Genomic library was screened and purified for further research including restriction mapping of ginseng mtDNA, and cloning of the genes. The gene of ATP synthase A subunit was cloned from the purified EMBL4 library clone No. 16. Now, clone No. 16 is subcloned for structure gene sequence analysis.

• Parasites, Hosts and Diseases
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• 제54권6호
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• pp.813-817
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• 2016

Armillifer agkistrodontis (Ichthyostraca: Pantastomida) is a parasitic pathogen, only reported in China, which can cause a zoonotic disease, pentastomiasis. A complete mitochondrial (mt) genome was 16,521 bp comprising 13 protein-coding genes (PCGs), 22 tRNA genes, 2 rRNA genes, and 1 non-coding region (NCR). A phylogenetic tree drawn with the concatenated amino acid sequences of the 6 conserved PCGs (atp6, cox1-3, and nad2) showed that A. agkistrodontis and Armillifer armillatus constituted a clade Pentastomida which was a sister group of the Branchiura. The complete mt genome sequence of A. agkistrodontis provides important genetic markers for both phylogenetic and epidemiological studies of pentastomids.

• 한국동물생명공학회지
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• 제35권1호
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• pp.102-111
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• 2020

Nitric oxide (NO)-induced protein S-nitrosylation triggers mitochondrial dysfunction and was related to cell senescence. However, the exact mechanism of these damages is not clear. In the present study, to investigate the relationship between in vitro aging and NO-induced protein S-nitrosylation, oocytes were treated with sodium nitroprusside dihydrate (SNP), and the resultant S-nitrosylated proteins were detected through biotin-switch assay. The results showed that levels of protein S-nitroso thiols (SNO)s and expression of S-nitrosoglutathione reductase (GSNOR) increased, while activity and function of mitochondria were impaired during oocyte aging. Addition of SNP, a NO donor, to the oocyte culture led to accelerated oocyte aging, increased mitochondrial dysfunction and damage, apoptosis, ATP deficiency, and enhanced ROS production. These results suggested that the increased NO signal during oocyte aging in vitro, accelerated oocyte degradation due to increased protein S-nitrosylation, and ROS-related redox signaling.

• Molecules and Cells
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• 제23권3호
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• pp.379-390
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• 2007

We sequenced and characterized the complete mitochondrial genome of the Japanese fish tapeworm D. nihonkaiense. The genome is a circular-DNA molecule of 13607 bp (one nucleotide shorter than that of D. latum mtDNA) containing 12 protein-coding genes (lacking atp8), 22 tRNA genes and two rRNA genes. Gene order and genome content are identical to those of the other cestodes reported thus far, including its congener D. latum. The only exception is Hymenolepis diminuta in which the positions of trnS2 and trnL1 are switched. We tested a PCR-based molecular assay designed to rapidly and accurately differentiate between D. nihonkaiense and D. latum using species-specific primers based on a comparison of their mtDNA sequences. We found the PCR-based system to be very reliable and specific, and suggest that PCR-based identification methods using mtDNA sequences could contribute to the study of the epidemiology and larval ecology of Diphyllobothrium species.

• Molecules and Cells
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• 제46권11호
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• pp.655-663
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• 2023

Autophagy dysfunction is associated with human diseases and conditions including neurodegenerative diseases, metabolic issues, and chronic infections. Additionally, the decline in autophagic activity contributes to tissue and organ dysfunction and aging-related diseases. Several factors, such as down-regulation of autophagy components and activators, oxidative damage, microinflammation, and impaired autophagy flux, are linked to autophagy decline. An autophagy flux impairment (AFI) has been implicated in neurological disorders and in certain other pathological conditions. Here, to enhance our understanding of AFI, we conducted a comprehensive literature review of findings derived from two well-studied cellular stress models: glucose deprivation and replicative senescence. Glucose deprivation is a condition in which cells heavily rely on oxidative phosphorylation for ATP generation. Autophagy is activated, but its flux is hindered at the autolysis step, primarily due to an impairment of lysosomal acidity. Cells undergoing replicative senescence also experience AFI, which is also known to be caused by lysosomal acidity failure. Both glucose deprivation and replicative senescence elevate levels of reactive oxygen species (ROS), affecting lysosomal acidification. Mitochondrial alterations play a crucial role in elevating ROS generation and reducing lysosomal acidity, highlighting their association with autophagy dysfunction and disease conditions. This paper delves into the underlying molecular and cellular pathways of AFI in glucose-deprived cells, providing insights into potential strategies for managing AFI that is driven by lysosomal acidity failure. Furthermore, the investigation on the roles of mitochondrial dysfunction sheds light on the potential effectiveness of modulating mitochondrial function to overcome AFI, offering new possibilities for therapeutic interventions.

• 대한약학회:학술대회논문집
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• 대한약학회 2002년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2
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• pp.262.1-262.1
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• 2002

Uncoupling proteins (UCPs) are transmembrane proton transporters present in the mitochondria. In UCPs. UCP1 and UCP3 play an important role in adaptive thermogenesis by uncoupling mitochondrial oxidation of substrates from ATP synthesis. PPARg coactivator 1(PGC-1) regulates transcriptional activity of PPARg and other nuclear receptors and controls the expression of UCPs. (omitted)

• Journal of Microbiology and Biotechnology
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• 제28권1호
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• pp.40-49
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• 2018

We evaluated the antioxidant activity and neuronal cell-protective effect of fucoidan extract from Ecklonia cava (FEC) on hydrogen peroxide ($H_2O_2$)-induced cytotoxicity in PC-12 and MC-IXC cells to assess its protective effect against oxidative stress. Antioxidant activities were examined using the ABTS radical scavenging activity and malondialdehyde-inhibitory effect, and the results showed that FEC had significant antioxidant activity. Intracellular ROS contents and neuronal cell viability were investigated using the DCF-DA assay and MTT reduction assay. FEC also showed remarkable neuronal cell-protective effect compared with vitamin C as a positive control for both $H_2O_2$-treated PC-12 and MC-IXC cells. Based on the neuronal cell-protective effects, mitochondrial function was analyzed in PC-12 cells, and FEC significantly restored mitochondrial damage by increasing the mitochondrial membrane potential (${\Delta}{\Psi}m$) and ATP levels and regulating mitochondrial-mediated proteins (p-AMPK and BAX). Finally, the inhibitory effects against acetylcholinesterase (AChE), which is a critical hydrolyzing enzyme of the neurotransmitter acetylcholine in the cholinergic system, were investigated ($IC_{50}$ value = 1.3 mg/ml) and showed a mixed (competitive and noncompetitive) pattern of inhibition. Our findings suggest that FEC may be used as a potential material for alleviating oxidative stress-induced neuronal damage by regulating mitochondrial function and AChE inhibition.

• 한국진공학회:학술대회논문집
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• 한국진공학회 2013년도 제44회 동계 정기학술대회 초록집
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• pp.199-199
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• 2013

The distinctive cellular and mitochondrial dysfunctions of a human epithelial lung cancer cell line (H460) from a human lung fibroblastic normal cell line (MRC5) have been studied by dielectric barrier discharge (DBD) plasma treatment. The DBD plasma device have generated large amount of H2O2 and NOx in culture media which is dependent on plasma exposure time. It is found that the cell number of lung cancer cell H460 has been reduced more than the lung normal cell MRC5 as being increased exposure and incubation time. Also these both cell lines have showed mitochondria fragmentation under 5 minutes' plasma exposure, which is a clue of apoptosis. It is noted in this study that AnnexinV staining has showed not only early apoptosis, but also late apoptosis in lung cancer cell H460. Mitochondria enzyme activity and ATP generation have been also much reduced in lung cancer cell H460. Their mitochondrial membrane potential (${\Delta}{\psi}m$) has been found to be reduced in magnitude and shifted to the induced-potential level of cccp, while MRC5 mitochondrial membrane potential has been shifted slightly to that. These distinctively selective responses of lung cancer cell H460 from lung normal cell MRC5 gives us possibility of applying plasma to cancer therapy.

• 한국수산과학회지
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• 제48권3호
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• pp.354-361
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• 2015

Mitochondrial heat shock protein 75 (mtHSP75) is a member of the HSP90 family and plays essential roles in refolding proteins of the mitochondrial matrix. Mitochondria provide energy in the form of ATP and generate reactive oxygen species (ROS). Heat shock proteins (HSPs) are activated in response to stress, and protect cells. In this study, we characterized the mtHSP75 of the big-belly seahorse Hippocampus abdominalis. The protein (BsmtHSP75) is encoded by an open reading frame (ORF) of 2,157 nucleotides, has 719 amino acids (aa), and is of molecular mass 82 kDa. BsmtHSP75 has two functional domains, a histidine kinase-like ATPase (HATPase_c) domain (123-276 aa) and an HSP90 family domain (302-718 aa). BsmtHSP75 was expressed in all tested tissues of healthy seahorses. The ovary contained the highest transcription level, followed (in order) by the blood, brain, and muscle. Pouch tissue showed the lowest expression level. The expression of BsmtHSP75 was significantly (P<0.05) up-regulated on viral or bacterial challenge, suggesting that BsmtHSP75 plays a role in the immune defense against bacterial and viral pathogens.

• Journal of Ginseng Research
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• 제46권5호
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• pp.646-656
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• 2022

Background: In addition to its use as a health food, ginseng is used in cosmetics and shampoo because of its extensive health benefits. The ginsenoside, Rh2, is a component of ginseng that inhibits tumor cell proliferation and differentiation, promotes insulin secretion, improves insulin sensitivity, and shows antioxidant effects. Methods: The effects of Rh2 on cell survival, extracellular matrix (ECM) protein expression, and cell differentiation were examined. The antioxidant effects of Rh2 in UV-irradiated normal human dermal fibroblast (NHDF) cells were also examined. The effects of Rh2 on mitochondrial function, morphology, and mitophagy were investigated in UV-irradiated NHDF cells. Results: Rh2 treatment promoted the proliferation of NHDF cells. Additionally, Rh2 increased the expression levels of ECM proteins and growth-associated immediate-early genes in ultraviolet (UV)-irradiated NHDF cells. Rh2 also affected antioxidant protein expression and increased total antioxidant capacity. Furthermore, treatment with Rh2 ameliorated the changes in mitochondrial morphology, induced the recovery of mitochondrial function, and inhibited the initiation of mitophagy in UV-irradiated NHDF cells. Conclusion: Rh2 inhibits mitophagy and reinstates mitochondrial ATP production and membrane potential in NHDF cells damaged by UV exposure, leading to the recovery of ECM, cell proliferation, and antioxidant capacity.