• Korea-Australia Rheology Journal
• /
• v.16 no.3
• /
• pp.141-146
• /
• 2004

Shear-induced damage of Red Blood Cell (RBC) is an imminent problem to be solved for the practical application of artificial organs in extra corporeal circulation, as it often happens and affects physiological homeostasis of a patient. To design and operate artificial organs in a safe mode, many investigations have been set up to correlate shear and shear-induced cell damage. Most studies were focused on hemolysis i.e. the extreme case, however, it is important as well to obtain a clear understanding of pre-hemolytic mechanical damage. In this study, the change in deformability of RBC was measured by ektacytometry to investigate the damage of RBC caused by shear. To a small magnitude of pre-shear, there is little difference, but to a large magnitude of pre-shear, cell damage occurs and the effect of shear becomes significant depending on both the magnitude and imposed time of shearing. The threshold stress for cell damage was found to be approximately 30 Pa, which is much less than the threshold of mechanical hemolysis but is large enough to occur in vitro as in the extra corporeal circulation during open-heart surgery or artificial heart. In conclusion, it was found and suggested that the decrease of deformability can be used as an early indication of cell damage, in contrast to measuring plasma hemoglobin. As cell damage always occurs during flow in artificial organs, the results as well as the approach adopted here will be helpful in the design and operation of artificial organs.

• International Journal of Industrial Entomology and Biomaterials
• /
• v.47 no.2
• /
• pp.90-98
• /
• 2023

The human eye, constantly exposed to solar radiation, can be damaged by UV radiation. In particular, ultraviolet B (UVB)-induced damage plays an important role in retinal degeneration and cell aging. In this study, we investigated the protective effects of the methanol extract of Oxya chinensis sinuosa (OCM), an edible insect known for its high protein content (64.2%), and various pharmacological effects, on human retinal pigment epithelial cells. ARPE-19 cells were treated with OCM and subsequently UVB irradiated. Our results showed that OCM effectively attenuates UVB-induced cell damage by reducing MAPK phosphorylation (JNK and p38 MAPK). Additionally, OCM increased the phosphorylation of Akt, and cell cycle regulators, including p21 and p27, in a dose-dependent manner. Moreover, OCM treatment increased ARPE-19 cell proliferation by activating the S6K1/S6 pathway. This study suggests that OCM prevents UVB-induced retinal cell damage by increasing cell proliferation via ROS reduction, suggesting its potential as a functional therapeutic superfood against retinal cell damage.

• Environmental Mutagens and Carcinogens
• /
• v.17 no.2
• /
• pp.71-77
• /
• 1997

The single cell gel electrophoressis(SCGE) assay, also known as the comet assay, is a rapid, simple, visual and sensitive technique for measuring and analysing DNA breakage in mammalian cells. The SCGE or comet assay is a promising test for the detection of DNA damage and repair in individnal cells. It has widespread potential applications in DNA damage and repair studies, genotoxicity testing and biomonitoring. In this microgel electrophoresis technique, cells are embedded in agarose gel on microscope slides, iysed and electrophoresed under alkaline conditions. Cells with increased DNA damage display increased migration of DNA from the nucleus towards the anode. The length of DNA migration indicates the amount of DNA breakage in the cell. The comet assay is also capable of identifying apoptotic cells which contain highly fragmented DNA. Here we review the development of the SCGE assay, existing protocols for the detection and analysis of comets, the relevant underlying principles determining the behaviour of DNA and the potential applications of the technique.

• Journal of The Korean Radiological Technologist Association
• /
• v.30 no.1
• /
• pp.70-76
• /
• 2004

To evaluate the process of radiation-induced cell damage in human promyelocytic leukemia cell HL-60 cell and chinese hamster cell CHO cell lines. I irradiated HL-60 cells, CHO cell line, using the V - radiation from Cs-137 cell irradiation(Gamma cell 3000

• Korean Journal of Plant Resources
• /
• v.21 no.6
• /
• pp.449-456
• /
• 2008

The flowers of Buddleja officinalis are used to treat sore and damaged eyes, a condition which is similar to skin wounds. However, whether it has any protective effect on oxidative DNA damage and cell death induced by hydroxyl radical remains unclear. In this study, we evaluated the protective effects of the extracts against oxidative DNA and cell damage caused by hydroxyl radical. DPPH radical, hydroxyl radical, hydrogen peroxide and intracellular ROS scavenging assay, and $Fe^{2+}$ chelating assay were used to evaluate the antioxidant properties. phi X 174 RF I plasmid DNA and intracellular DNA migration assay were used to evaluate the protective effect against oxidative DNA damage. Lastly, MTT assay and lipid peroxidation assay were used to evaluate the protective effect against oxidative cell damage. It was found to prevent intracellular DNA and the normal cells from oxidative damage caused by hydroxyl radical via antioxidant activities. These results suggest that Buddleja officinalis may exert the inhibitory effect on ROS-induced carcinogenesis by blocking oxidative DNA damage and cell death.

• Journal of Preventive Medicine and Public Health
• /
• v.37 no.4
• /
• pp.373-380
• /
• 2004

Objectives : There has been gradually increasing concern about the adverse health effects of electromagnetic radiation originating from cell phones which are widely used in modern life. Cell phone radiation may affect human health by increasing free radicals of human blood cells. This study has been designed to identify DNA damage of blood cells by electromagnetic radiation caused by cell phone use. Methods : This study investigated the health effect of acute exposure to commercially available cell phones on certain parameters such as an indicator of DNA damage for 14 healthy adult volunteers. Each volunteer during the experiment talked over the cell phone with the keypad facing the right side of the face for 4 hours. The single cell gel electrophoresis assay (Comet assay), which is very sensitive in detecting the presence of DNA strand-breaks and alkali-labile damage in individual cells, was used to assess peripheral blood cells (T-cells, B-cells, granulocytes) from volunteers before and after exposure to cell phone radiation. The parameters of Comet assay measured were Olive Tail Moment and Tail DNA %. Results : The Olive Tail Moment of B-cells and granulocytes and Tail DNA % of B-cells and granulocytes were increased by a statistically significant extent after 4-hour use of a cell phone compared with controls. Conclusion : It is concluded that cell phone radiation caused the DNA damage during the 4 hours of experimental condition. Nonetheless, this study suggested that cell phone use may increase DNA damage by electromagnetic radiation and other contributing factors.

• Molecules and Cells
• /
• v.19 no.2
• /
• pp.167-179
• /
• 2005

The cells of metazoans respond to DNA damage by either arresting their cell cycle in order to repair the DNA, or by undergoing apoptosis. This response is highly conserved across species, and many of the genes involved in this DNA damage response have been shown to be inactivated in human cancers. This suggests the importance of DNA damage response with regard to the prevention of cancer. The DNA damage checkpoint responses vary greatly depending on the developmental context, cell type, gene expression profile, and the degree and nature of the DNA lesions. More valuable information can be obtained from studies utilizing whole organisms in which the molecular basis of development has been well established, such as Drosophila. Since the discovery of the Drosophila p53 orthologue, various aspects of DNA damage responses have been studied in Drosophila. In this review, I will summarize the current knowledge on the DNA damage checkpoint response in Drosophila. With the ease of genetic, cellular, and cytological approaches, Drosophila will become an increasingly valuable model organism for the study of mechanisms inherent to cancer formation associated with defects in the DNA damage pathway.

• Molecular & Cellular Toxicology
• /
• v.1 no.2
• /
• pp.111-115
• /
• 2005

Ultraviolet (UV) radiation to mammalian skin is known to alter cellular function via generation of Reactive Oxygen Species (ROS), DNA damage and DNA lesions, such as pyrimidine dimmers and photoproducts, which could lead to DNA mutation if they are not repaired. In this study, we have investigated the reduction of DNA damage and of apoptosis with a particular attention to genetic effect of paeoniflorin in Normal Human Epidermal Keratinocytes (NHEK). After UVB irradiation from $10\;to\;500mJ/cm^{2}$ to NHEK, Mean Tail Moments (MTM) were increased with UVB dose increase. The greatest amount of strand breaks was induced at $500mJ/cm^{2}$ of UVB. Even at the lowest dose of UVB ($10mJ/cm^{2}$), change in MTM was detected (P<0.0001). Pretreated cell with 0.1% paeoniflorin maximally reduced the level of DNA damage to about 21.3%, compared to untreated cell. In the lower concentrations less than 0.01% of paeoniflorin, MTM had a small increase but paeoniflorin still had reductive effects of DNA damage. We measured the apoptosis suppression of paeoniflorin with annexin V flous staining kit. As we observed under the fluorescence microscopy to detect apoptosis in the irradiated cell, the fluorescence intensity was clearly increased in the untreated cell, but decreased in treated cells with paeoniflorin. These results suggest that paeoniflorin reduces the alteration of cell membranes and prevents DNA damage. Therefore, the use of paeoniflorin as a free radical scavenger to reduce the harmful effects of UV lights such as chronic skin damage, wrinkling and skin cancer can be useful to prevent the formation of photooxidants that result in radical damage.

• Proceedings of the Korean Society of Toxicology Conference
• /
• 2006.11a
• /
• pp.55-64
• /
• 2006

The fetal central nervous system (CNS) is sensitive to diverse environmental factors, such as alcohol, heavy metals, irradiation, mycotoxins, neurotransmitters, and DNA damage, because a large number of processes occur during an extended period of development. Fetal neural damage is an important issue affecting the completion of normal CNS development. As many concepts about the brain development have been recently revealed, it is necessary to compare the mechanism of developmental abnormalities induced by extrinsic factors with the normal brain development. To clarify the mechanism of fetal CNS damage, we used one experimental model in which 5-azacytidine (5AZC), a DNA damaging and demethylating agent, was injected to the dams of rodents to damage the fetal brain. 5AzC induced cell death (apoptosis)and cell cycle arrest in the fetal brain, and it lead to microencephaly in the neonatal brain. We investigated the mechanism of apoptosis and cell cycle arrest in the neural progenitor cells in detail, and demonstrated that various cell cycle regulators were changed in response to DNA damage. p53, the guardian of genome, played a main role in these processes. Further, using DNA microarray analysis, tile signal cascades of cell cycle regulation were clearly shown. Our results indicate that neural progenitor cells have the potential to repair the DNA damages via cell cyclearrest and to exclude highly affected cells through the apoptotic process. If the stimulus and subsequent DNA damage are high, brain development proceeds abnormally and results in malformation in the neonatal brain. Although the mechanisms of fetal brain injury and features of brain malformation afterbirth have been well studied, the process between those stages is largely unknown. We hypothesized that the fetal CNS has the ability to repair itself post-injuring, and investigated the repair process after 5AZC-induced damage. Wefound that the damages were repaired by 60 h after the treatment and developmental processes continued. During the repair process, amoeboid microglial cells infiltrated in the brain tissue, some of which ingested apoptotic cells. The expressions of genes categorized to glial cells, inflammation, extracellular matrix, glycolysis, and neurogenesis were upregulated in the DNA microarray analysis. We show here that the developing brain has a capacity to repair the damage induced by the extrinsic stresses, including changing the expression of numerous genes and the induction of microglia to aid the repair process.

• Biomolecules & Therapeutics
• /
• v.31 no.3
• /
• pp.340-349
• /
• 2023

Mad2B (Mad2L2), the human homolog of the yeast Rev7 protein, is a regulatory subunit of DNA polymerase ζ that shares sequence similarity with the mitotic checkpoint protein Mad2A. Previous studies on Mad2B have concluded that it is a mitotic checkpoint protein that functions by inhibiting the anaphase-promoting complex/cyclosome (APC/C). Here, we demonstrate that Mad2B is activated in response to cisplatin-induced DNA damage. Mad2B co-localizes at nuclear foci with DNA damage markers, such as proliferating cell nuclear antigen and gamma histone H2AX (γ-H2AX), following cisplatin-induced DNA damage. However, unlike Mad2A, the binding of Mad2B to Cdc20 does not inhibit the activity of APC/C in vitro. In contrast to Mad2A, Mad2B does not localize to kinetochores or binds to Cdc20 in spindle assembly checkpoint-activated cells. Loss of the Mad2B protein leads to damaged nuclei following cisplatin-induced DNA damage. Mad2B/Rev7 depletion causes the accumulation of damaged nuclei, thereby accelerating apoptosis in human cancer cells in response to cisplatin-induced DNA damage. Therefore, our results suggest that Mad2B may be a critical modulator of DNA damage response.