• Biomaterials Research
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• v.22 no.4
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• pp.221-234
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• 2018

Background: Interest in subcellular organelle-targeting theranostics is substantially increasing due to the significance of subcellular organelle-targeting drug delivery for maximizing therapeutic effects and minimizing side effects, as well as the significance of theranostics for delivering therapeutics at the correct locations and doses for diseases throughout diagnosis. Among organelles, mitochondria have received substantial attention due to their significant controlling functions in cells. Main body: With the necessity of subcellular organelle-targeting drug delivery and theranostics, examples of mitochondria-targeting moieties and types of mitochondria-targeting theranostics were introduced. In addition, the current studies of mitochondria-targeting theranostic chemicals, chemical conjugates, and nanosystems were summarized. Conclusion: With the current issues of mitochondria-targeting theranostic chemicals, chemical conjugates, and nanosystems, their potentials and alternatives are discussed.

• BMB Reports
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• v.56 no.2
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• pp.90-95
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• 2023

Mitochondria are important organelles that regulate adenosine triphosphate production, intracellular calcium buffering, cell survival, and apoptosis. They play therapeutic roles in injured cells via transcellular transfer through extracellular vesicles, gap junctions, and tunneling nanotubes. Astrocytes can secrete numerous factors known to promote neuronal survival, synaptic formation, and plasticity. Recent studies have demonstrated that astrocytes can transfer mitochondria to damaged neurons to enhance their viability and recovery. In this study, we observed that treatment with mitochondria isolated from rat primary astrocytes enhanced cell viability and ameliorated hydrogen peroxide-damaged neurons. Interestingly, isolated astrocytic mitochondria increased the number of cells under damaged neuronal conditions, but not under normal conditions, although the mitochondrial transfer efficiency did not differ between the two conditions. This effect was also observed after transplanting astrocytic mitochondria in a rat middle cerebral artery occlusion model. These findings suggest that mitochondria transfer therapy can be used to treat acute ischemic stroke and other diseases.

• The Korean Journal of Pharmacology
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• v.14 no.1_2
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• pp.1-11
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• 1978

The $Na^+$-and $K^+$-induced $Ca^{++}$ release was measured isotopically by Milipore filter technique in mitochondria isolated from rabbit ventricles. The release of $Ca^{++}$ from mitochondria could be induced by 1-3 mM of $Na^+$ added in incubating medium under the presence of 0.5mM EGTA to prevent the released $Ca^{++}$ from rebinding with mitochondrial membrane. The amount of $Ca^{++}$ released was increased by increasing the concentration of $Na^+$ added. 100mM $K^+$, in itself, did not induce the $Ca^{++}$ release from cardiac mitochondria, the $Na^+$-induced $Ca^{++}$ release, however, was potentiated by the presence of $K^+$. The potentiation of $Na^+$-induced $Ca^{++}$ release by $K^+$ was proportional to the $Na^+/K^+$ ratio presented in the incubating medium. Among the monovalent cations other than $Na^+$, the release of $Ca^{++}$ from cardiac mitochondria was shared only by $Li^+$. The $Na^+$-induced $Ca^{++}$ release could be also observed in the mitochondria isolated from liver and kidney. However, the $Na^+$ sensitivity was somewhat lower in liver and kidney mitochondria than in heart mitochondria. The release of $Ca^{++}$ induced by $Na^+$ in the mitochondria isolated from the experimentally produced failured heart was not different from that in the normal heart mitochondria, and was not directly modified by $10^{-6}{\sim}10^{-5}$ M of Ouabain. From the experiments, it was suggested that the $Ca^{++}$ released from mitochondria by $Na^+$ could be used in excitation-contraction coupling process to initiate the contraction of the cardiac myofibrils. Futhermore, it appeared that the phenomenon of $Ca^{++}$ release from cardiac mitochondria by $Na^+$ and $K^+$ might be related to the inotropic effect of digitalis glycoside which could bring about the increase of $Na^+$ or the reduction of $K^+$ intracellulary through the inhibition of $Na^+$, $K^+$-ATPase.

• Proceedings of the KSAR Conference
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• 2001.03a
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• pp.11-11
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• 2001

In this study, we examined the developmental potential of reconstructed bovine embryos and the fate of donor mitochondria during their preimplantation development after nuclear transfer. Isolated cumulus cells were used as donor cells in nuclear transfer. Cumulus cells labelled with MitoTracker Green FM fluorochrome were injected into enucleated bovine MII oocytes and cultured in vitro. MitoTracker labelling on donor cells did not have a detrimental effect on blastocyst formation following nuclear transfer. Cleavage rate was about 69%(56/81) and blastocyst formation rate was 6.2% (5/81) at 7 days after nuclear transfer. The labelled mitochondria dispersed to the cytoplasm and became distributed among blastomeres and could be identified up to the 8- to 15-cell stages. Small patches of mitochondria were detected in some 8- to 15-cell stage embryos (5/20). However, donor mitochondria were not detected in embryos at the 16-cell stage and subsequent developmental stages. In the control group, mitochondria could be identified in arrested 1-cell embryos up to 7 days after nuclear transfer These results suggest that donor mitochondria disappear from recipient cytoplasm before 16-cell stage following nuclear transfer in reconstructed bovine embryos.

• Clinical and Experimental Reproductive Medicine
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• v.50 no.1
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• pp.1-11
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• 2023

In reproduction, mitochondria produce bioenergy, help to synthesize biomolecules, and support the ovaries, oogenesis, and preimplantation embryos, thereby facilitating healthy live births. However, the regulatory mechanism of mitochondria in oocytes and embryos during oogenesis and embryo development has not been clearly elucidated. The functional activity of mitochondria is crucial for determining the quality of oocytes and embryos; therefore, the underlying mechanism must be better understood. In this review, we summarize the specific role of mitochondria in reproduction in oocytes and embryos. We also briefly discuss the recovery of mitochondrial function in gametes and zygotes. First, we introduce the general characteristics of mitochondria in cells, including their roles in adenosine triphosphate and reactive oxygen species production, calcium homeostasis, and programmed cell death. Second, we present the unique characteristics of mitochondria in female reproduction, covering the bottleneck theory, mitochondrial shape, and mitochondrial metabolic pathways during oogenesis and preimplantation embryo development. Mitochondrial dysfunction is associated with ovarian aging, a diminished ovarian reserve, a poor ovarian response, and several reproduction problems in gametes and zygotes, such as aneuploidy and genetic disorders. Finally, we briefly describe which factors are involved in mitochondrial dysfunction and how mitochondrial function can be recovered in reproduction. We hope to provide a new viewpoint regarding factors that can overcome mitochondrial dysfunction in the field of reproductive medicine.

• ALGAE
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• v.21 no.3
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• pp.323-332
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• 2006

Mitochondrial distribution and abundance were assessed during the growth of apical and subapical cells in the red algae Colaconema caespitosum (J. Agardh) Jackelman, Stegenga and Bolton and Antithamnion cruciatum (C. Agardh) Nägeli after staining with 3,3’-dihexyloxacarbocyanine iodide [DiOC6(3)] and 2,4’-dimethylaminostyryl-Nethylpyridinium iodide (DASPEI). In fully elongate apical cells of C. caespitosum there were 100-120 mitochondria. During apical cell enlargement and division there is a doubling and then halving of the mitochondrial numbers. Apical cells prior to cytokinesis in young filaments are smaller than in mature filaments (ca. 50 and 100 μm long, respectively) and have fewer mitochondria (ca. 100 and 120 mitochondria per cell, respectively). In older vegetative cells mitochondria tend to aggregate at opposite ends of the cells with some mitochondria associated with the central nucleus or at points of apparent branch initiation. There is a greater density of mitochondria in apical cells of smaller versus larger plants (one mitochondrion per 6.3 μm3 and 9.8 μm3, respectively), suggesting that apical cells of younger plants may be more metabolically active. Male and female gametophytic thalli of Antithamnion cruciatum had similar numbers of mitochondria in apical cells of indeterminate axes, as did gametophytic and sporophytic thalli. There were about 40-50 mitochondria in fully elongated apical cells with about half this number in newly divided apical and subapical cells. Apical cells of determinate branches had more mitochondria (60-77) than indeterminate branches (60-70 vs. 40-50). In both species and in all cell types mitochondrial numbers were highly correlated with cell size.

• BMB Reports
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• v.44 no.8
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• pp.517-522
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• 2011

Mitochondrial dynamics not only involves mitochondrial morphology but also mitochondrial biogenesis, mitochondrial distribution, and cell death. To identify specific regulators to mitochondria dynamics, we screened a chemical library and identified niclosamide as a potent inducer of mitochondria fission. Niclosamide promoted mitochondrial fragmentation but this was blocked by down-regulation of Drp1. Niclosamide treatment resulted in the disruption of mitochondria membrane potential and reduction of ATP levels. Moreover, niclosamide led to apoptotic cell death by caspase-3 activation. Interestingly, niclosamide also increased autophagic activity. Inhibition of autophagy suppressed niclosamide-induced cell death. Therefore, our findings suggest that niclosamide induces mitochondria fragmentation and may contribute to apoptotic and autophagic cell death.

• BMB Reports
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• v.51 no.11
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• pp.549-556
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• 2018

Mitochondria are ubiquitous and multi-functional organelles involved in diverse metabolic processes, namely energy production and biomolecule synthesis. The intracellular mitochondrial morphology and distribution change dynamically, which reflect the metabolic state of a given cell type. A dramatic change of the mitochondrial dynamics has been observed in early development that led to further investigations on the relationship between mitochondria and the process of development. A significant developmental process to focus on, in this review, is a differentiation of neural progenitor cells into neurons. Information on how mitochondria-regulated cellular energetics is linked to neuronal development will be discussed, followed by functions of mitochondria and associated diseases in neuronal development. Lastly, the potential use of mitochondrial features in analyzing various neurodevelopmental diseases will be addressed.

• Korean Journal of Microbiology
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• v.2 no.1
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• pp.12-16
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• 1964

Lee, Yung Nok and Chin, Pyung (Dept. of Biology, Korea University, Seoul, Korea) : Action of ascorbic acid indoleacetic acid on the oxidation of succinate and coupled phosphorylation in Chlorella mitochondria. Kor. Jour. Microbiol., Vol.2, No.1, p12-16 (1964) Mitochondria were isolated from Chlorella ellipsoidea and the action of ascorbic acid and indoleacetic acid on the succinate oxidation and coupled phosphorylation in mitochondria suspension were examined. Oxidation of succinate used as substrate, and phosphorylation coupled to oxidation were strikingly enhanced by the addition of ascorbic acid, while in case of indoleacetic acid it were a little. In a view of phosphorylative efficiency, P/O ratio resulting from the addition of ascorbic acid was decreased and it may be considered as the result of a partial oxidation of ascorbate in mitochondria.

• Toxicological Research
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• v.31 no.4
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• pp.323-330
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• 2015

Cancer is a disease characterized by uncontrolled growth. Metabolic demands to sustain rapid proliferation must be compelling since aerobic glycolysis is the first as well as the most commonly shared characteristic of cancer. During the last decade, the significance of metabolic reprogramming of cancer has been at the center of attention. Nonetheless, despite all the knowledge gained on cancer biology, the field is not able to reach agreement on the issue of mitochondria: Are damaged mitochondria the cause for aerobic glycolysis in cancer? Warburg proposed the damaged mitochondria theory over 80 years ago; the field has been testing the theory equally long. In this review, we will discuss alterations in metabolic fluxes of cancer cells, and provide an opinion on the damaged mitochondria theory.