• Proceedings of the Zoological Society Korea Conference
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• 1997.10b
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• pp.211.1-211
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• 1997

No Abstract, See Full Text

• Toxicological Research
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• v.13 no.1_2
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• pp.61-69
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• 1997

Exposure of splenocytes to 2-chloroethylethyl sulfide (CEES) resulted in the cell death, and the cytotoxicity of CEES was prevented by inhibitors of lysosomal hydrolases. Therefore, it has been postulated that the cytotoxicity of CEES may be partially due to the lysosomal labilization. This study, based on this mechanism, was undertaken to determine whether aminoglycoside antibiotics as inhibitors of lysosomal phospholipases and their combinations with other lysosome stabilizers can be useful as a treatment to reduce the CEES toxicity in mice. 2-Chloroethylethyl sulfide (20 mg/kg body weight) was injected ip into female ICR mice, and candidate compounds were administered ip before or after the CEES challenge. Kanamycin (40 mg/kg body weight) as effective as deferoxamine (100 mg/kg body weight) enhanced the survival rate after 5 days of intoxication from 10% of control to 50 - 60%. The most effective was found to be the combination of kanamycin, cycloheximide, deferoxamine and dextrose showing an almost full protection against 2LD50 of CEES. Consistent with the protection of the CEES toxicity, the decrease of body weight in mice intoxicated with CEES was effectively prevented by kanamycin or its combinations. It is suggested that kanamycin or its combination (kanamycin, cycloheximide, deferoxamine and dextrose) would be one of effective antidotes against the CEES poisoning in mice.

• Applied Microscopy
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• v.30 no.2
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• pp.165-172
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• 2000

To investigate the defensive effect of green tea against the lead toxicity, Sprague-Dewley rats (150 gm) were divided into 5 groups; the control group, the group treated with lead for 4 weeks (Group A-1), the group treated with lead and green tea for 4 weeks (Group A-2), the group treated with lead for 8 weeks (Group B-1), and the group treated with lead and green tea for 8 weeks (Group B-2). The lead acetate (500 ppm) was injected two times for one week into the abdomen and green tea solution (3 g/100 ml distilled water) offered freely. In the liver cell, The cristae of mitochondria were enlarged, the rough endoplasmic reticulum (rER) extended and many lysosome observed on the Group A- 1. The cristae of mitochondria were enlarged and many lysosome observed, but nucleus was normal on the Croup A-2. All of observed parts on the Group B-1 deeply wounded by lead than the group A-1. In the Group B-2, the mitochondria and rER were increased in number than the Group B-1 and the nucleus was observed normally.

• Applied Microscopy
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• v.40 no.1
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• pp.15-19
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• 2010

The present study was designed to demonstrate ionic zinc in the rat DRG by means of zinc selenium autometallography($ZnSe^{AMG}$). Ganglion cells varied in size from 15 to 100 ${\mu}m$. The smaller neurons were strongly stained with AMG, whereas the larger cells were weakly stained. Each large ganglion cell was surrounded by perineuronal satellite cells, showing apparent AMG staining. We demonstrated for the first time the existence of zinc-containing satellite cells in the rodent DRG. Using electron microscopy, fine AMG grains were observed scattered in the somata of the DRG neurons, especially small cells. However, much lower concentrations of the AMG grains occupied in the large cells, and these were mostly localized in lysosome-like organelles. These results indicate that zinc may be involved in sensory transmission in the DRG level.

• Development and Reproduction
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• v.16 no.2
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• pp.129-135
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• 2012

Previously, we identified that the overexpression of IEX-1 induces apoptosis in ovarian cancer cells. Herein we report a new binding partner of IEX-1, CATHEPSIN B, as a lysosomal enzyme which contributes to the various apoptotic signaling in tumor cells. To investigate how IEX-1 regulates cellular survival and death event, we performed yeast two-hybrid screening of rat ovarian cDNA library using IEX-1 as the bait and found CATHEPSIN B. In the present study, CATHEPSIN B and IEX-1 proteins were overexpressed in 293T cells and their specific association was determined by immunoprecipitation and immunoblot analysis. In addition, the endogenous interaction between CATHEPSIN B and IEX-1 was confirmed in HeLa cells. The current finding of lysosomal CATHEPSIN B as the IEX-1-binding partner implies that IEX-1 may involve in lysosome-mediated apoptotic signaling pathways.

• The Korean Journal of Zoology
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• v.28 no.3
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• pp.151-165
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• 1985

The morphological changes of the midgut epithelium during the metamorphosis of pine caterpillar are observed with light and electron microscope, being divided into 5 stages from the 8th instar larva to just after pupation. The midgut epithelium of 8th instar larva is composed of columnar cell, goblet cell, regenerative cell, and endocrine cell. The secretorials are arranged on the nuclear membrane in the columnar cell of the midgut epithelium in the 8th instar larva, and lysosomes are augmented in the apical portion. Cytoplasmic extrusions are observed in the apical surface of columnar cell but they have no cell organells. Nucleus, mitochondria, rER, Golgi complex, and free ribsomes are observed in the regenerative cell. Regenerative cells are differentiated into the form of goblet cell, and vacuoles are gradually increased in the cytoplasm. Just pupa stage, the materials, which appears to be mainly composed of Ca, are observed in the circular form and goblet cavity of regenerative cell are detached to lumen. As a result, it reflects the process of the degeneration of the midgut epithelium that lysosomes are gradually augmented in the columnar cell, that nuclear materials are removed to cytoplasm, and that cytoplasmic extrusions are observed in the apical surface. And though regenerative cells are differentiated into the form of the goblet cell, it is believed that goblet cavity is detached from regenerative cell to the lumen and midgut epithelium of pupa stage is formed.

• Molecules and Cells
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• v.43 no.12
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• pp.989-1001
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• 2020

Salmonella enterica serovar Typhimurium (S. Typhimurium) is a facultative intracellular pathogen that causes salmonellosis and mortality worldwide. S. Typhimurium infects macrophages and survives within phagosomes by avoiding the phagosome-lysosome fusion system. Phagosomes sequentially acquire different Rab GTPases during maturation and eventually fuse with acidic lysosomes. Lysophosphatidylcholine (LPC) is a bioactive lipid that is associated with the generation of chemoattractants and reactive oxygen species (ROS). In our previous study, LPC controlled the intracellular growth of Mycobacterium tuberculosis by promoting phagosome maturation. In this study, to verify whether LPC enhances phagosome maturation and regulates the intracellular growth of S. Typhimurium, macrophages were infected with S. Typhimurium. LPC decreased the intracellular bacterial burden, but it did not induce cytotoxicity in S. Typhimurium-infected cells. In addition, combined administration of LPC and antibiotic significantly reduced the bacterial burden in the spleen and the liver. The ratios of the colocalization of intracellular S. Typhimurium with phagosome maturation markers, such as early endosome antigen 1 (EEA1) and lysosome-associated membrane protein 1 (LAMP-1), were significantly increased in LPC-treated cells. The expression level of cleaved cathepsin D was rapidly increased in LPC-treated cells during S. Typhimurium infection. Treatment with LPC enhanced ROS production, but it did not affect nitric oxide production in S. Typhimurium-infected cells. LPC also rapidly triggered the phosphorylation of IκBα during S. Typhimurium infection. These results suggest that LPC can improve phagosome maturation via ROS-induced activation of NF-κB pathway and thus may be developed as a therapeutic agent to control S. Typhimurium growth.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.12 no.1
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• pp.5-13
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• 2012

I-cell disease (mucolipidosis type II; MIM 252500) and pseudo-Hurler polydystrophy (mucolipidosis type III; MIM 252600) are disorders caused by abnormal lysosomal transport in cells. The presence of numerous inclusion bodies in the cytoplasm of fibroblasts, a lack of mucopolysacchariduria, increased lysosomal enzyme activity in serum, and decreased GlcNAc-phosphotransferase activity are hallmark. Here, we attempted to investigate phenotypical and biochemical characteristics of the knockoutmouse of GlcNAc-phosphotransferase ${\alpha}/{\beta}$ subunits; in addition, we also attempted to determine whether the lysosome enriched fraction derived from placenta can be beneficial to phenotype and biochemistry of the knockout mouse.We found that the knockout mouse failed to thrive and had low bone density, as is the case in human. In addition, skin fibroblasts from the animal had the same biochemical characteristics, including increased lysosomal enzyme activity in the culture media, in contrast to the relatively low enzyme activity within the cells. Intravenous injection of the lysosome rich fraction derived from placenta into the tail vein of the animal resulted in a gain of weight, while saline injected animals didn't.In conclusion, our study demonstrated the phenotypical and biochemical similarities of the knockout mouse to a mucolipidosis type II patient and showed the therapeutic potential of the lysosome enriched fraction. We admit that a larger scale animal study will be needed; however, the disease model and the therapeutic potential of the lysosome enriched fraction will highlight the hope for a novel treatment approach to mucopolipidosis type II, for which no therapeutic modality is available.

• BMB Reports
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• v.42 no.2
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• pp.65-71
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• 2009

Autophagy, which is a process of self eating, has gained interest in the past decade due to its both beneficial and controversial roles in various biological phenomena. The discovery of autophagy genes (ATG) in yeast has led to focused research designed to elucidate the mechanism and regulation of this process. The role of autophagy in a variety of biological phenomena, including human disease, is still the subject of debate. However, recent findings suggest that autophagy is a highly regulated process with both beneficial and negative effects. Indeed, studies conducted using various model organisms have demonstrated that increased autophagy leads to an extended lifespan. Despite these findings, it is still unknown if all pathways leading to extended lifespan converge at the process of autophagy or not. Here, an overview of modern developments related to the process of autophagy, its regulation and the molecular machinery involved is presented. In addition, this review focuses on one of the beneficial aspects of autophagy, its role in lifespan regulation.

• Applied Microscopy
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• v.18 no.2
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• pp.119-131
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• 1988

The purpose of this study was to investigate the differentiation and degeneration of neurons in developing chick embryo. The activity of acid phosphatase(ACP) was measured and cytochemical study of ACP and ultrastructural changes were observed in prosencephalon, mesencephalon and rhombencephalon from day 4 to day 19 of incubation. As a result, the activity of ACP of all brain region was tend to increase from day 4 to day 19. On day 13, activities of ACP of mesencephalon and rhombencephalon were increased greatly and activity of ACP was decreased each region on day 17. On electron microscopic examination, the reaction product of ACP were localized at GERL complex, lysosome, Golgi body and vacuoles of neurons. Morphologically, disrupted nuclear envelope, mitochondrial destruction, vacuolization and ribosomal crystalization were observed.