• Molecules and Cells
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• v.28 no.3
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• pp.139-148
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• 2009

Cell death has been traditionally classified in apoptosis and necrosis. Apoptosis, known as programmed cell death, is an active form of cell death mechanism that is tightly regulated by multiple cellular signaling pathways and requires ATP for its appropriate process. Apoptotic death plays essential roles for successful development and maintenance of normal cellular homeostasis in mammalian. In contrast to apoptosis, necrosis is classically considered as a passive cell death process that occurs rather by accident in disastrous conditions, is not required for energy and eventually induces inflammation. Regardless of different characteristics between apoptosis and necrosis, it has been well defined that both are responsible for a wide range of human diseases. Glycogen storage disease type I (GSD-I) is a kind of human genetic disorders and is caused by the deficiency of a microsomal protein, glucose-6-phosphatase-${\alpha}$ ($G6Pase-{\alpha}$) or glucose-6-phosphate transporter (G6PT) responsible for glucose homeostasis, leading to GSD-Ia or GSD-Ib, respectively. This review summarizes cell deaths in GSD-I and mostly focuses on current knowledge of the neutrophil apoptosis in GSD-Ib based upon ER stress and redox signaling.

• Korean Journal of Veterinary Service
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• v.25 no.3
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• pp.295-297
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• 2002

This experiment was done to set up the immunohistochemical detection method for infectious hematopoietic necrosis virus(IHNV) antigens in the monolayers of CHSE-214 cell cultures inoculated with IHNV. Specific identification of IHNV antigens was detected in the cytoplasms of infected cells by the use of monoclonal antibodies to glycoproteins. The specific positive signal was observed as a distinct red color. The result showed that streptavidin alkaline phosphatase immunohistochemistry specifically identified IHNV antigens in infected cultured cells.

• BMB Reports
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• v.41 no.1
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• pp.1-10
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• 2008

Surgery, Chung-Ang Unviersity College of Medicine, Yong-San Hospital, Seoul, Korea Apoptosis is considered to be a programmed and controlled mode of cell death, whereas necrosis has long been described as uncontrolled and accidental cell death resulting from extremely harsh conditions. In the following review, we will discuss the features and physiological meanings as well as recent advances in the elucidation of the signaling pathways of both apoptotic cell death and programmed necrotic cell death.

• Biomolecules & Therapeutics
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• v.22 no.3
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• pp.167-175
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• 2014

Chemotherapy has long been considered as one of useful strategies for cancer treatment. It is primarily based on the apoptosis that can selectively kill cancer cells. However, cancer cells can progressively develop an acquired resistance to apoptotic cell death, rendering refractory to chemo- and radiotherapies. Although the mechanism by which cells attained resistance to drug remains to be clarified, it might be caused by either pumping out of them or interfering with apoptotic signal cascades in response to cancer drugs. In case that cancer cells are defective in some part of apoptotic machinery by repeated exposure to anticancer drugs, alternative cell death mechanistically distinct from apoptosis could be adopted to remove cancer cells refractory to apoptosis-inducing agents. This review will mainly deal with harnessing of necrotic cell death, specifically, programmed necrosis and practical uses. Here, we begin with various defects of apoptotic death machinery in cancer cells, and then provide new perspective on programmed necrosis as an alternative anticancer approach.

• Journal of Microbiology and Biotechnology
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• v.26 no.4
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• pp.790-798
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• 2016

Chlamydiae, obligate intracellular bacteria, are associated with a variety of human diseases. The chlamydial life cycle undergoes a biphasic development: replicative reticulate bodies (RBs) phase and infectious elementary bodies (EBs) phase. At the end of the chlamydial intracellular life cycle, EBs have to be released to the surrounded cells. Therefore, the interactions between Chlamydiae and cell death pathways could greatly influence the outcomes of Chlamydia infection. However, the underlying molecular mechanisms remain elusive. Here, we investigated host cell death after Chlamydia infection in vitro, in L929 cells, and showed that Chlamydia infection induces cell necrosis, as detected by the propidium iodide (PI)-Annexin V double-staining flow-cytometric assay and Lactate dehydrogenase (LDH) release assay. The production of reactive oxygen species (ROS), an important factor in induction of necrosis, was increased after Chlamydia infection, and inhibition of ROS with specific pharmacological inhibitors, diphenylene iodonium (DPI) or butylated hydroxyanisole (BHA), led to significant suppression of necrosis. Interestingly, live-cell imaging revealed that Chlamydia infection induced lysosome membrane permeabilization (LMP). When an inhibitor upstream of LMP, CA-074-Me, was added to cells, the production of ROS was reduced with concomitant inhibition of necrosis. Taken together, our results indicate that Chlamydia infection elicits the production of ROS, which is dependent on LMP at least partially, followed by induction of host-cell necrosis. To our best knowledge, this is the first live-cell-imaging observation of LMP post Chlamydia infection and report on the link of LMP to ROS to necrosis during Chlamydia infection.

• BMB Reports
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• v.31 no.2
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• pp.183-188
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• 1998

2-chloroethylethyl sulfide (CEES) is an alkylating agent that readily reacts with a wide variety of biological molecules causing metabolic abnormality. The mechanism of cell death during CEES injury is poorly understood. We have examined the effect of exposure of thymocytes with various concentrations of CEES to determine the pattern of cell death in thymocytes injury induced by CEES. In the present study, we show that two patterns of cell death occurred by either one of two mechanisms: apoptosis and necrosis. Exposure to low level of CEES (100 ${\mu}M$) for 5 h caused an induction of apoptosis on thymocytes, as identified by the following criteria: DNA fragmentation visualized by the characteristic "ladder" pattern was observed upon agarose gel electrophoresis and morphological features were revealed by microscopical observations. In contrast, exposure to high levels of CEES (500 ${\mu}M$) induce necrotic features such as cell lysis. Thus, depending on the concentrations, CEES can result in either apoptotic or necrotic cell damage. Our findings suggest that thymocytes which are not killed directly, but merely injured by low levels of CEES, are able to activate an internally-programmed cell death mechanism, whereas thymocytes receiving severe damages apparently can not.

• Journal of Korean Academy of Oral and Maxillofacial Radiology
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• v.11 no.1
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• pp.33-40
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• 1981

The author studied on the effects of x-irradiation to the development of digital malformation in gestation rats. The time-matings occured between 6 p.m. and 8 a.m. and females with copulation. plugs at 8 a.m. were isolated and properly marked for evidence of copulation. The lower abdomen of mothers were exposed to x-irradiation on the 11½th day of gestation, the critical period developing digital malformation, respectively 100, 150, 200, 250, 300 and 350 rads. At 18½th day of post-conception total 50 pregnant females were dissected and the incidence of digital malformations were obtained. Rat embryos on the 12, 13, 14, 15, 16th day of gestation irradiated by 250 rads were examined for morphogenesis of digital malformation. Digital radiating lines were examined in water and histologically by H-E stain. Supra vital stain samples by Nile-blue sulfate in 37℃ normal saline were prepared for the observation of cell necrosis regions and morphogenesis of digits. The results obtained were as follows; 1. By x-irradiation on 11th day of gestation, digital malformations of Ectrodactylia, Syndactylia Polydactylia and Hematodactylia were developed. Ectrodactylia showed the effective relationship to the amount of irradiation, however Syndactylia ans Polydactylia did not. 2. By x-irradiation, cell necrosis of digital germ was appeared markedly, but in 48 hours after irradiation was depressed to the periphery of digital germ and in 72hours after irradiation was disappeared. Digital radiating line showed marked stage of malformation in 48hours after irradiation and continued to show the same amount of physiological cell necrosis as the compared control group in 72hours. after irradiaion. But in the Syndactylia, physiological cell necrosis was not able to be recognized. 3. Ectrodactylia induced by x-irradiation was considered as the direct resoult of cell necrosis of digital origin, however, Polydactylia and Syndactylia were considered as the resoult of some effect in repair process of x-irradiation damages.

• Journal of Biomedical Engineering Research
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• v.25 no.1
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• pp.49-55
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• 2004

In this paper, we investigated the effects of the photodynamic therapy(PDT) for the tumor mass in mice. In the experimental method, we divided the mice into two control and test group which HepG2 and HeLa cell line induced cancer mass in mice. Photofrin was administered to the tumor-bearing mouse, followed 30 hours later by 630nm and 650nm laser light exposure. After photodynamic therapy we analyzed the two mice group for the tumor mass size, tumor growth, tumor cell necrosis, pathological anatomy change. According to the results, tumor cell necrosis was shown in the tissues which the reduce size of tumor and tumor cell necrotic change according to the irradiation time and light dose amount. The considerable difference, however, between the 630nm and 650nm wavelength was not found for the tumor cell necrotic change and other damage of normal tissue was not found.

• Microbiology and Biotechnology Letters
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• v.50 no.3
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• pp.387-394
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• 2022

Verotoxin-1 (VT-1) or Shiga-like toxin 1 (Stx-1) is produced by enterohemorrhagic Escherichia coli (EHEC) and is an AB5 holotoxin with a strong inhibitor of protein synthesis. VT-1 is a type 2 ribosome-inactivating protein (RIP) that has been shown to have cytotoxic and anticancer potential by inducing necrosis, apoptosis, and cell cycle arrest, making it a promising antitumor candidate. Here, we tested the cytotoxicity of VT-1 on CaCo2 and NCM425 cell lines and the results showed that VT-1 was more potent on CaCo2. Morphological changes were also evaluated on the cellular level and the results showed that VT-1 caused a decrease in viable cell count, altered cell membrane permeability, and an increase in total nuclear intensity. On the other hand, VT-1 displayed a lesser impact on mitochondrial membrane potential (MMP) and cytochrome c release. On the expression of caspases 3 and 9, VT-1 exhibited an insignificant effect on both which alongside the mitochondrial membrane potential (MMP) and cytochrome c results, might indicate that CaCo2 suffered from the necrosis process as a mechanism of cell death after exposure to VT-1.

• Korean Journal of Veterinary Pathology
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• v.3 no.1
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• pp.1-5
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• 1999

This experiment was carried out to establish the immunohistochemical diagnostic method for infectious pancreatic necrosis in the monolayers of CHSE-214 cell cultures and paraffin-embedded tissue sections from rainbow trout infected with infectious pancreatic necrosis virus(IPNV). Specific identification of IPNV antigens was often demonstrated in the pancreatic exocrine cells, and less in the intestinal mucous epithelia and the renal hemopoietic tissues by the use of monoclonal antibodies against capsid protein VP2. The specific reaction was seen as a distinct red cytoplasmic color, often as small granules of various sizes. The result showed that streptavidin alkaline phosphatase immunohistochemisry specifically identified IPNV antigens in both infected cell cultures and tissue sections.