• 아시안잔디학회지
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• 제11권1호
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• pp.59-72
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• 1997

The influence of respiration on photosythetic electron transport were investigated in the Wid type and psaB mutants from Syneehocystis sp. PCC6803. The amount of glucose uptake in the wild type was proportional to the glucose concentration added in wild type and less than that of psaB mutants in the dark. It was suggested that psaB mutants more depend on the glucose than the wild type. It was investigated how the activities of isocitrate dehydrogenase(IDH) and glucose-6-phos-phate dehydrogenase(G6PDH) were changed. The activities of IDH were very low. While, the ac-tivities of G6PDH were much higher than that of IDH. These results agree to the reports that ex-ogenous glucose was dismilated aerobically via Oxidative Pentose Phosphate Pathway in heterotrophic cyanobacteria. PsaB mutants showed high G6PDH activity in the presence of glucose as well as in the dark and high respiratory activities especially in the dark. It was also investigated how photosynthetic electron transport activities were changed. PsaB mutants showed higher photosynthetic electron tranasport activities than wild type in the presence of glucose as well as in the dark. In the results, it was proposed that photosynthetic electron transport between PS I and PS U was complemented by respiratory electron transport through the NADPH generated by Dxidative Pentose Phophate Pathway in psaB mutant from Synechocystis sp. PCC6803. Key words: Photosynthetic electron transport, Respiration, Synechoystis sp. PCC6803, psaB mutant, Glucose uptake, IDH, G6PDH, Respiratory electron transport activity.

• 한국식품영양과학회지
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• 제20권5호
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• pp.409-417
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• 1991

To investigate effects of chronic alcohol consumption and tocopherol on lipid peroxidation and mitochondrial respiration 48 male rats of Sprague-Dawley strain were divided into 4 groups. Each group received for 3 weeks one of 4 experimental diets: tocopherol deficient control (TDC), tocopherol deficient-ethanol (TDE), tocopherol-supplemented control (TSC) and tocopherol-supplemented-ethanol (TSE). Composition of the diets was based on the Lieber and Decarli liquid diet and $\alpha$-tocopherol was supplemented at the level of 30mg/liter of diet, and ethanol supplied 36kcal%. TDC and TSC were pair-fed to TDE and TSE, respectively. Increase of body weight of tocopherol deficient-ethanol group was the lowest and the effect was diminished with tocopherol supplementation. Respiration of liver mitochondria was depressed in ethanol-administered groups and the effect became larger with tocopherol deficiency. Hepatic lipid peroxide level was not influenced by ethanol, but hepatic tocopherol content decreased with ethanol treatment. The result indicated that, although lipid perroxide level was unchanged with chronic ethanol consumption, oxidative stress exists in tissues of rate administered ethanol and may be relieved by tocopherol supplementation.

• The Korean Journal of Physiology and Pharmacology
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• 제19권3호
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• pp.283-289
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• 2015

This study surveys the improvement characteristics in old-aged muscular mitochondria by bio-active materials coated fabric (BMCF). To observe the effects, the fabric (10 and 30%) was worn to old-aged rat then the oxygen consumption efficiency and copy numbers of mitochondria, and mRNA expression of apoptosis- and mitophagy-related genes were verified. By wearing the BMCF, the oxidative respiration significantly increased when using the 30% materials coated fabric. The mitochondrial DNA copy number significantly decreased and subsequently recovered in a dose-dependent manner. The respiratory control ratio to mitochondrial DNA copy number showed a dose-dependent increment. As times passed, Bax, caspase 9, PGC-$1{\alpha}$ and ${\beta}$-actin increased, and Bcl-2 decreased in a dose-dependent manner. However, the BMCF can be seen to have had no effect on Fas receptor. PINK1 expression did not change considerably and was inclined to decrease in control group, but the expression was down-regulated then subsequently increased with the use of the BMCF in a dose-dependent manner. Caspase 3 increased and subsequently decreased in a dose-dependent manner. These results suggest that the BMCF invigorates mitophagy and improves mitochondrial oxidative respiration in skeletal muscle, and in early stage of apoptosis induced by the BMCF is not related to extrinsic death-receptor mediated but mitochondria-mediated signaling pathway.

• Toxicological Research
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• 제30권4호
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• pp.235-242
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• 2014

Cancer cells are known to drastically alter cellular energy metabolism. The Warburg effect has been known for over 80 years as pertaining cancer-specific aerobic glycolysis. As underlying molecular mechanisms are elucidated so that cancer cells alter the cellular energy metabolism for their advantage, the significance of the modulation of metabolic profiles is gaining attention. Now, metabolic reprogramming is becoming an emerging hallmark of cancer. Therapeutic agents that target cancer energy metabolism are under intensive investigation, but these investigations are mostly focused on the cytosolic glycolytic processes. Although mitochondrial oxidative phosphorylation is an integral part of cellular energy metabolism, until recently, it has been regarded as an auxiliary to cytosolic glycolytic processes in cancer energy metabolism. In this review, we will discuss the importance of mitochondrial respiration in the metabolic reprogramming of cancer, in addition to discussing the justification for using mitochondrial DNA somatic mutation as metabolic determinants for cancer sensitivity in glucose limitation.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-1
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• pp.108-111
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• 2003

Parkinson's disease (PD) is a common neurodegenerative disorder characterized by a progressive loss of dopaminergic neurons in the substantia nigra. While its precise etiology is unknown, such factors as oxidative stress, impairment of mitochondrial respiration, excitotoxicity and inflammation may play roles in its pathogenesis. Although the role of apoptosis in the process of dopaminergic neuronal death has been highlighted in studies using postmortem brains and experimental models of PD, other evidence implicates both apoptosis and non-apoptotic death in PD. (omitted)

• BMB Reports
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• 제49권2호
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• pp.116-121
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• 2016

Although proteomic analyses have revealed the presence of mitochondrial oxidative phosphorylation (OXPHOS) proteins in the plasma membrane, there have been no in-depth evaluations of the presence or function of OXPHOS I-V in the plasma membrane. Here, we demonstrate the in situ localization of OXPHOS I-V complexes to the sarcolemma of skeletal muscle by immunofluorescence and immunohistochemistry. A portion of the OXPHOS I-V complex proteins was not co-stained with MitoTracker but co-localized with caveolin-3 in the sarcolemma of mouse gastrocnemius. Mitochondrial matrix-facing OXPHOS complex subunits were ectopically expressed in the sarcolemma of the non-permeabilized muscle fibers and C2C12 myotubes. The sarcolemmal localization of cytochrome c was also observed from mouse gastrocnemius muscles and C2C12 myotubes, as determined by confocal and total internal resonance fluorescence (TIRF) microscopy. Based on these data, we conclude that a portion of OXPHOS complexes is localized in the sarcolemma of skeletal muscle and may have non-canonical functions.

• Journal of Community Nutrition
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• 제7권3호
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• pp.163-168
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• 2005

The present investigation was undertaken in vivo to determine whether the functional alterations of hepatic mitochondria induced by ethanol might be prevented by taurine. We examined the effects of supplementation of taurine on hepatic mitochondrial oxidative phosphorylation in the chronic ethanol-administered rats. Isolated hepatic mitochondria from three groups of rats were functionally tested by an analysis of $\beta-hydroxbutyrate-supported$ respiration and the coupling of this process to ATP synthesis in the presence of ADP. The three groups were control group(CO), ethanol(60g/L) administered group (AL), and ethanol (60g/L) + taurine (5g/L) supplemented group (AT). Ethanol and/or taurine were given in drinking water for 10 weeks. The mitochondria from AL group had lower state 4 respiratory rate, respiratory control (RC) ratio and ADP : O(P/O) ratio than those from CO and AT group. It showed that the ethanol administered rats were less coupled and thus less efficient with respect to mitochondrial ATP synthesis than both control rats and ethanol + taurine supplemented rats. It suggests that taurine supplementation might improve the impaired oxidative phosphorylation efficiency in mitochondrial dysfunction that is recognized as a cause of liver diseases in chronic ethanol consumption.

• Journal of Ginseng Research
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• 제43권4호
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• pp.517-526
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• 2019

Background: The root of Panax ginseng, a member of Araliaceae family, has been used as herbal medicine and functional food in Asia for thousands of years. According to Traditional Chinese medicine, ginseng is the most widely used "Qi-invigorating" herbs, which provides tonic and preventive effects by resisting oxidative stress, influencing energy metabolism, and improving mitochondrial function. Very few reports have systematically measured cell mitochondrial bioenergetics after ginseng treatment. Methods: Here, H9C2 cell line, a rat cardiomyoblast, was treated with ginseng extracts having extracted using solvents of different polarity, i.e., water, 50% ethanol, and 90% ethanol, and subsequently, the oxygen consumption rate in healthy and tert-butyl hydroperoxideetreated live cultures was determined by Seahorse extracellular flux analyzer. Results: The 90% ethanol extracts of ginseng possessed the strongest antioxidative and tonic activities to mitochondrial respiration and therefore provided the best protective effects to H9C2 cardiomyocytes. By increasing the spare respiratory capacity of stressed H9C2 cells up to three-folds of that of healthy cells, the 90% ethanol extracts of ginseng greatly improved the tolerance of myocardial cells to oxidative damage. Conclusion: These results demonstrated that the low polarity extracts of ginseng could be the best extract, as compared with others, in regulating the oxygen consumption rate of cultured cardiomyocytes during mitochondrial respiration.

• Molecules and Cells
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• 제41권1호
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• pp.35-44
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• 2018

Mitochondria are responsible for supplying of most of the cell's energy via oxidative phosphorylation. However, mitochondria also can be deleterious for a cell because they are the primary source of reactive oxygen species, which are generated as a byproduct of respiration. Accumulation of mitochondrial and cellular oxidative damage leads to diverse pathologies. Thus, it is important to maintain a population of healthy and functional mitochondria for normal cellular metabolism. Eukaryotes have developed defense mechanisms to cope with aberrant mitochondria. Mitochondria autophagy (known as mitophagy) is thought to be one such process that selectively sequesters dysfunctional or excess mitochondria within double-membrane autophagosomes and carries them into lysosomes/vacuoles for degradation. The power of genetics and conservation of fundamental cellular processes among eukaryotes make yeast an excellent model for understanding the general mechanisms, regulation, and function of mitophagy. In budding yeast, a mitochondrial surface protein, Atg32, serves as a mitochondrial receptor for selective autophagy that interacts with Atg11, an adaptor protein for selective types of autophagy, and Atg8, a ubiquitin-like protein localized to the isolation membrane. Atg32 is regulated transcriptionally and post-translationally to control mitophagy. Moreover, because Atg32 is a mitophagy-specific protein, analysis of its deficient mutant enables investigation of the physiological roles of mitophagy. Here, we review recent progress in the understanding of the molecular mechanisms and functional importance of mitophagy in yeast at multiple levels.

• The Korean Journal of Physiology and Pharmacology
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• 제21권6호
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• pp.567-577
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• 2017

Obesity is known to induce inhibition of glucose uptake, reduction of lipid metabolism, and progressive loss of skeletal muscle function, which are all associated with mitochondrial dysfunction in skeletal muscle. Mitochondria are dynamic organelles that regulate cellular metabolism and bioenergetics, including ATP production via oxidative phosphorylation. Due to these critical roles of mitochondria, mitochondrial dysfunction results in various diseases such as obesity and type 2 diabetes. Obesity is associated with impairment of mitochondrial function (e.g., decrease in $O_2$ respiration and increase in oxidative stress) in skeletal muscle. The balance between mitochondrial fusion and fission is critical to maintain mitochondrial homeostasis in skeletal muscle. Obesity impairs mitochondrial dynamics, leading to an unbalance between fusion and fission by favorably shifting fission or reducing fusion proteins. Mitophagy is the catabolic process of damaged or unnecessary mitochondria. Obesity reduces mitochondrial biogenesis in skeletal muscle and increases accumulation of dysfunctional cellular organelles, suggesting that mitophagy does not work properly in obesity. Mitochondrial dysfunction and oxidative stress are reported to trigger apoptosis, and mitochondrial apoptosis is induced by obesity in skeletal muscle. It is well known that exercise is the most effective intervention to protect against obesity. Although the cellular and molecular mechanisms by which exercise protects against obesity-induced mitochondrial dysfunction in skeletal muscle are not clearly elucidated, exercise training attenuates mitochondrial dysfunction, allows mitochondria to maintain the balance between mitochondrial dynamics and mitophagy, and reduces apoptotic signaling in obese skeletal muscle.