• Restorative Dentistry and Endodontics
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• 제21권1호
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• pp.385-402
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• 1996

Cytotoxicity of dental restorative materials using cell culture technique has been extensively studied by various quantitative assays. The aim of this study was to investigate the microstructural change of damaged L292 cells which could not observed with light microscope. Cytotoxic effect of ZOE, Prisma APH (Densply International Inc., U.S.A.), Clearfil FII(Kuraray Co., Japan), Fuji II(GC Co., Japan) and Fuji II LC(GC Co., Japan) on cultured L292 cells were observed. Irreversible cell damage and cytolysis were found in ZOE and Fuji II groups. In Clearfil FII, mild to moderate cell damage was observed. APH group showed variable cytotoxicity. Moderate cell damage was found in Fuji II LC group. Cytotoxic effect were as follows : A condensation of the chromatin occureds along or adjacent to the inner membrane of the nuclear envelops. The nuclear envelope remained resonably intact but the contents were partially or completely lost. The cell nucleus contains clusters of markedly electron-dense interchromatin granules. The rough endoplasmic reticulum were dilated. In some mitochondira, matrix was disoriented and fused cristae were discernible. Mitochondiral swelling and woolly appearance were recognized. Large vacuoles and autolysosmes were found in cytoplasm. Some breaks of the cytoplasmic membrane and even cytolysis could be seen in dying cells.

• Journal of Microbiology and Biotechnology
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• 제19권10호
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• pp.1122-1126
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• 2009

The exogenously added cadaverine is effective in protecting Vibrio vulnificus from methyl viologen (MV)-induced superoxide stress at pH 8.5. Such a protective effect by cadaverine was not observed at pH 7.5. Consistently, the accumulated level of intracellular cadaverine at pH 8.5 is approximately four times as much as that of the control cell at pH 7.5. Cadaverine accumulation is not affected by MV. The protection of V. vulnificus by cadaverine from superoxide stress was abolished when cadB coding for the lysine-cadaverine antiporter was interrupted. However, the cadaverine-mediated protection was complemented with cadB DNA. Therefore, CadB of V. vulnificus not only acts as a lysine-cadaverine antiporter at acid pH to neutralize the external medium, but also mediates cadaverine uptake at alkaline pH to result in cell protection from superoxide stress.

• The Korean Journal of Physiology and Pharmacology
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• 제12권2호
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• pp.65-71
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• 2008

The present study examined the inhibitory effect of licorice compounds glycyrrhizin and a metabolite $18{\beta}$-glycyrrhetinic acid on the neurotoxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in the mouse and on the 1-methyl-4-phenylpyridinium ($MPP^+$)-induced cell death in differentiated PC12 cells. MPTP treatment increased the activities of total superoxide dismutase, catalase and glutathione peroxidase and the levels of malondialdehyde and carbonyls in the brain compared to control mouse brain. Co-administration of glycyrrhizin (16.8 mg/kg) attenuated the MPTP effect on the enzyme activities and formation of tissue peroxidation products. In vitro assay, licorice compounds attenuated the $MPP^+$-induced cell death and caspase-3 activation in PC12 cells. Glycyrrhizin up to $100{\mu}M$ significantly attenuated the toxicity of $MPP^+$. Meanwhile, $18{\beta}$-glycyrrhetinic acid showed a maximum inhibitory effect at $10{\mu}M$; beyond this concentration the inhibitory effect declined. Glycyrrhizin and $18{\beta}$-glycyrrhetinic acid attenuated the hydrogen peroxide- or nitrogen species-induced cell death. Results from this study indicate that glycyrrhizin may attenuate brain tissue damage in mice treated with MPTP through inhibitory effect on oxidative tissue damage. Glycyrrhizin and $18{\beta}$-glycyrrhetinic acid may reduce the $MPP^+$ toxicity in PC12 cells by suppressing caspase-3 activation. The effect seems to be ascribed to the antioxidant effect.

• Molecules and Cells
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• 제19권3호
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• pp.382-390
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• 2005

Calcium-binding proteins are thought to play important roles in calcium buffering. The present study investigated the effects of ischemia and reperfusion on calbindin D28K, calretinin, and parvalbumin immunoreactivity in the ganglion cell layer of the rabbit. Rabbits were administered ischemic damage by increasing the intraocular pressure. After 60 and 90 min of ischemia, reperfusion (7 d) was allowed to occur. The b-wave of the electroretinogram (ERG) was reduced by more than 50% and almost 80% in retina given ischemia for 60 and 90 min, respectively. The oscillatory potential (OPs) wave was reduced approximately 50% at 60 min ischemia and 70% at 90 min ischemia. In both normal and ischemic-treated retina, calcium-binding protein immunoreactivity was seen in many cells in the ganglion cell layer. In eyes subjected to 60 min ischemia, there was a decrease of the density of calbindin D28K- (8.29%), calretinin- (14.44%), and parvalbumin- (26.83%) immunoreactive (IR) cells compared to the control retina. In eyes subjected to 90 min ischemia, there was a higher decrease of the density of calbindin D28K- (18.48%), calretinin- (33.59%), and parvalbumin- (54.26%) IR cells than at 60 min. Some calcium-binding protein-IR neurons, especially calretinin-IR neurons, showed aggregations that were abnormally packed together in retina subjected to ischemia for 90 min. The results show that calbindin D28K-, calretinin-, and parvalbumin-IR cells in the ganglion cell layer are susceptible to ischemic damage and reperfusion. The degree of reduction varied among different calcium-binding proteins and ischemic damage times. These results suggest that calbindin D28K-containing neurons are less susceptible to ischemic damage than calretinin- and parvalbumin-containing neurons in the ganglion cell layer of rabbit retina.

• 한국환경성돌연변이발암원학회지
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• 제22권2호
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• pp.83-89
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• 2002

The single cell gel electrophoresis (comet) assay is one of the useful tools for the study of genetic damage in humans exposed to environmental mutagens and carcinogens. This study was undertaken to evaluate the status of DNA damage in peripheral lymphocytes depending on their sex, age, smoking habits, and other factors in normal healthy Korean population. The 99 volunteers included in the study and out of these, 36 volunteers were smoker and 63 volunteers were non-smoker aged between 20-59 years. All individual answered a questionnaire that assessed their general information including smoking habits and the extent of the environmental tobacco smoke (ETS) exposure, and blood samples were obtained. There was a statistically significant difference in the extent of DNA damage between smoker and non-smoker (p<0.001). A significant difference was also observed between male and female (p<0.001) and amongst the different group of age (p<0.005), however, correlation analysis showed that only smoking habit was a significant factor for DNA damage. No significant effect of smoking duration, number of cigarettes smoking a day, SPY (smoke pack years) in smokers and environmental tobacco smoke exposure in non-smokers on the status of DNA damage was observed.

• BMB Reports
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• 제47권5호
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• pp.249-255
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• 2014

Polo-like kinase-1 (Plk1) belongs to a family of serine-threonine kinases and plays a critical role in mitotic progression. Plk1 involves in the initiation of mitosis, centrosome maturation, bipolar spindle formation, and cytokinesis, well-reported as traditional functions of Plk1. In this review, we discuss the role of Plk1 during DNA damage response beyond the functions in mitotsis. When DNA is damaged in cells under various stress conditions, the checkpoint mechanism is activated to allow cells to have enough time for repair. When damage is repaired, cells progress continuously their division, which is called checkpoint recovery. If damage is too severe to repair, cells undergo apoptotic pathway. If damage is not completely repaired, cells undergo a process called checkpoint adaptation, and resume cell division cycle with damaged DNA. Plk1 targets and regulates many key factors in the process of damage response, and we deal with these subjects in this review.

• Journal of Animal Science and Technology
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• 제63권5호
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• pp.984-997
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• 2021

This study sought to evaluate DNA damage and repair in porcine postovulatory aged oocytes. The DNA damage response, which was assessed by H2A.X expression, increased in porcine aged oocytes over time. However, the aged oocytes exhibited a significant decrease in the expression of RAD51, which reflects the DNA damage repair capacity. Further experiments suggested that the DNA repair ability was suppressed by the downregulation of genes involved in the homologous recombination (HR) and nonhomologous end-joining (NHEJ) pathways. The expression levels of the cell cycle checkpoint genes, CHEK1 and CHEK2, were upregulated in porcine aged oocytes in response to induced DNA damage. Immunofluorescence results revealed that the expression level of H3K79me2 was significantly lower in porcine aged oocytes than in control oocytes. In addition, embryo quality was significantly reduced in aged oocytes, as assessed by measuring the cell proliferation capacity. Our results provide evidence that DNA damage is increased and the DNA repair ability is suppressed in porcine aged oocytes. These findings increase our understanding of the events that occur during postovulatory oocyte aging.

• 한국환경성돌연변이발암원학회지
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• 제21권2호
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• pp.135-141
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• 2001

Endocrine disruptors have been implicated in carcinogenesis in animal studies, but carcinogenetic effects on human remain controversial. In order to examine the genotoxicity of two common endocrine disruptors, Bisphenol A and Diethylstilbestrol, cytogenetic endpoints including chromosome aberration (CA), sister chromatid exchange (SCE), micronuclei (MN) analyses and DNA damage by single cell gel electrophoresis (SCGE) were assessed. The effects of Bisphenol A and Diethylstilbestrol on the frequencies of CA and MN were increased in a dose-dependent manner and that of Bispheol A was more significant by Kendall'$\tau$test. Bisphenol A and Diethylstilbestrol also increased the frequency of SCE. Bisphenol A and Diethylstilbestrol induced DNA damage in a dose-dependent manner and the DNA damage induced by Diethylstilbestrol in human blood lymphocytes was more significant.

• 대한통합의학회지
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• 제11권2호
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• pp.169-179
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• 2023

Purpose : Although human periodontal ligament stem cells (hPDLSCs) are a supportive factor for tissue engineering, oxidative stress during cell culture and transplantation has been shown to affect stem cell viability and mortality, leading to failed regeneration. The aim of this study was to evaluate the antioxidant and protective effects against cell damage of celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, and the antioxidant signal of hPDLSCs in H₂O₂-induced oxidative stress. Methods : To induce oxidative stress in cultured hPDLSCs, H₂O₂ was used as an exogenous reactive oxygen species (ROS). Dose-dependent celecoxib (.1, 1, 10, or 100 µM) was administered after H₂O₂ treatment. WST-1 assay was used to assess cell damage and western blot was used to observe antioxidant activity of hPDLSCs in oxidative stress. Immunohistochemistry was performed for inverting the localization of the SOD and Nrf2 antibody. Results : We found that progressive cell death was induced in hPDLSCs by H₂O₂ treatment. However, low-dose celecoxib reduced H₂O₂-induced cellular damage and eventually enhanced the SOD activity and Nrf2 signal of hPDLSCs. Oxidative stress-induced morphological change in hPDLSCs included lowered the survival and number of spindle-shaped cells, and shrinkage and shortening of cell fibers. Notably, celecoxib promoted cell survival function and activated antioxidants such as SOD and Nrf2 by positively regulating the cell survival signal pathway, and also reduced the number of morphological changes in hPDLS. Immunohistochemistry results showed a greater number of SOD- and Nrf2-stained cells in the celecoxib-treated group following oxidative stress. Conclusion : By increasing SOD and Nrf2 expression at the antioxidant system, the findings suggest that celecoxib enhanced the antioxidative ability of hPDLSCs and protected cell viability against H₂O₂-induced oxidative stress by increasing SOD and Nrf2 expression in the antioxidant system.

• 대한한의학회지
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• 제23권4호
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• pp.113-124
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• 2002

Objects: This research was conducted to investigate the protective effect of Bupleuri Radix against ischemic damage using PC12 cells and global ischemia in gerbils, Methods: To observe the protective effect of Bupleuri Radixon ischemic damage, viability and changes in activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase and production of malondialdehyde (MDA) were observed after treating PC12 cells with Bupleuri Radix during ischemic damage. Gerbils were divided into three groups: a normal group, a 5-minute two-vessel occlusion (2VO) group and a Bupleun Radix administered group after 2VO. The CCAs were occluded by microclip for 5 minutes, Bupleuri Radix was administered orally for 7 days after 2VO. Histological analysis was performed on the 7th day. For histological analysis, the brain tissue was stained with 1 % of cresyl violet solution. Results: 1. Bupleuri Radix has a protective effect against ischemia in the CA1 area of the gerbil's hippocampus 7 days after 5-minute occlusion. 2. In the hypoxia/reperfusion model using PC12 cells, the Bupleuri Radix has a protective effect against ischemia in the dose of 0.2{\;}\mu\textrm{g}/ml,2{\;}\mu\textrm{g}/ml{\;}and{\;} 20{\;}\mu\textrm{g}/ml$. 3. Bupleuri Radix increased the activities of glutathione peroxidase and catalase. 4. The increased activity of superoxidedismutase (SOD) by ischemic damage might have been induced as an act of self-protection. This study suggests that Bupleuri Radix has some neuroprotective effect against neuronal damage following cerebral ischemia in vivo with a widely used experimental model of cerebral ischemia in Mongolian gerbils. Bupleuri Radix also has protective effect on a hypoxia/reperfusion cell culture model using PC12 cells. Conclusions: Bupleuri Radix has protective effect against ischemic brain damage during the early stages of ischemia.