• Journal of the Korean Association of Oral and Maxillofacial Surgeons
• /
• v.34 no.5
• /
• pp.509-517
• /
• 2008

DNA damage accumulates in cells as a result of exposure to exogenous agents such as benzopyrene, cigarette smoke, ultraviolet light, X-ray, and endogenous chemicals including reactive oxygen species produced from normal metabolic byproducts. DNA damage can also occur during aberrant DNA processing reactions such as DNA replication, recombination, and repair. The major of DNA damage affects the primary structure of the double helix; that is, the bases are chemically modified. These modification can disrupt the molecules'regular helical structure by introducing non-native chemical bonds or bulky adducts that do not fit in the standard double helix. DNA repair genes and proteins scan the global genome to detect and remove DNA damage and damage to single nucleotides. Direct reversal of DNA damage, base excision repair, double strand break. DNA repair are known relevant DNA repair mechanisms. Four different mechanisms are distinguished within excision repair: direct reversal, base excision repair, nucleotide excision repair, and mismatch repair. Genetic variation in DNA repair genes can modulate DNA repair capacity and alter cancer risk. The instability of a cell to properly regulate its proliferation in the presence of DNA damage increase risk of gene mutation and carcinogenesis. This article aimed to review mechanism of excision repair and to understand the relationship between genetic variation of excision repair genes and head and neck cancer.

• Journal of Photoscience
• /
• v.9 no.2
• /
• pp.479-481
• /
• 2002

UV-induced DNA damage causes cell killing and mutations leading to carcinogenesis. In normal human cells, UV damage such as cyclobutane pyrimidine dimers (CPDs) and primidine-prymidone (6-4) photoproducts are mainly repaired by nucleotide excision repair mechanism. The molecular processes have been well characterized recently. To know the influence of mitochondrial genome on the nucleotide excision repair mechanism against CPDs, we comparatively examined the production of CPDs by UVC irradiation and their repair kinetics in human cells completely lacking mitochondrial DNA (mtDNA) and the parental HeLa S cells. Whole DNA extracted from the cells exposed to UVC was treated with T4-endonuclease V to break the phosphodiester bond adjacent to CPDs. The DNA was electrophoresed in a denaturing agarose gel, which was visualized by ethidium bromide staining. The relative amount of CPDs was determined by image analysis using NIH Image software. MtDNA- less (rho-O) cells were apparently more sensitive to UVC than HeLa S cells, while the level of induction of CPDs in rho-O and HeLa cells was comparable. The repair of CPDs was less efficient in rho-O cells compared with HeLa cells. The residual amount of CPDs after 24-h repair was larger in rho-O cells than in HeLa cells where more than 90 % of CPDs were repaired by then. The non-repaired CPDs would lead to apoptosis in rho-O cells. These results suggest that mitochondrial genome may contribute to some ATP-dependent steps in nucletide excision repair by supplying sufficient ATP which is generated through a respiratory chain in mitochondria.

• Animal cells and systems
• /
• v.9 no.2
• /
• pp.79-85
• /
• 2005

Oxidized abasic residues arise as a major class of DNA damage by a variety of agents involving free radical attack and oxidation of deoxyribose sugar components. 2-deoxyribonolactone (dL) is a C1'-oxidized abasic lesion implicated in DNA strand scission, mutagenesis, and covalent DNA-protein cross-link (DPC). We show here that mammalian cell-free extract give rise to stable DPC formation that is specifically mediated by dL residue. When a duplex DNA containing dL at the site-specific position was incubated with cell-free extracts of Po ${\beta}-proficient$ and -deficient mouse embryonic fibroblast cells, the formation of major dL-mediated DPC was dependent on the presence of DNA polymerase (Pol) ${\beta}$. Formation of dL-specific DPC was also observed with histones and FEN1 nuclease, although the reactivity in forming dL-mediated DPC was significantly higher with Pol ${\beta}$ than with histones or FEN1. DNA repair assay with a defined DPC revealed that the dL lesion once cross-linked with Pol ${\beta}$ was resistant to nucleotide excision repair activity of cell-free extract. Analysis of nucleotide excision repair utilizing a model DNA substrate containing a (6-4) photoproduct suggested that excision process for DPC was inhibited because of DNA single-strand incision at 5' of the lesion. Consequently DPC mediated by dL lesion may not be readily repaired by DNA excision repair pathway but instead function as unusual DNA damage causing a prolonged DNA strand break and trapping of the major base excision repair enzyme.

• Biomedical Science Letters
• /
• v.11 no.2
• /
• pp.103-108
• /
• 2005

2-Deoxyribonolactone (dL) arises as a major DNA damage induced by a variety of agents, involving free radical attack and oxidation of C1'-deoxyribose in DNA. We investigated whether dL lesions can be repaired in mammalian cells and the mechanisms underlying the role of DNA polymerase $\beta$ in processing of dL lesions. Pol $\beta$ appeared to be trapped by dL residues, resulting in stable DNA-protein cross-links. However, repair DNA synthesis at site-specific dL sites occurred effectively in cell-free extracts, but predominantly accompanied by long-patch base excision repair (BER) pathway. Reconstitution of long-patch BER demonstrated that FEN1 was capable of removing the displaced flap DNA containing a 5'-dL residue. Cellular repair of dL lesions was largely dependent on the DNA polymerase activity of Pol $\beta$. Our observations reveal repair mechanisms of dL and define how mammalian cells prevent cytotoxic effects of oxidative DNA lesions that may threaten the genetic integrity of DNA.

• Archives of Craniofacial Surgery
• /
• v.18 no.4
• /
• pp.277-281
• /
• 2017

Traumatic cleft earlobes are a common problem encountered by plastic and reconstructive surgeons. Various techniques have been reported for the repair of traumatic cleft earlobes. Usually, the techniques of split earlobe repair are divided into two categories, namely straight- and broken-line repairs. Straight-line repair is simple and easy, but scar contracture frequently results in notching of the inferior border of the lobule. It can be avoided by the broken-line repair such as Z-plasty, L-plasty, or a V-shaped flap. Between April 2016 and February 2017, six patients who presented with traumatic cleft earlobe underwent surgical correction using a combination of the inverted V-shaped excision technique and vertical mattress suture method. All the patients were female and had a unilateral complete cleft earlobe. No postoperative notching of the inferior border the lobule occurred during 6-16 months of follow-up. Without the use of a broken-line repair, both the patients and the operators attained aesthetically satisfactory results. Therefore, the combination of the inverted V-shaped excision technique and vertical mattress suture method is considered useful in the treatment of traumatic cleft earlobes.

• The Korean Journal of Zoology
• /
• v.23 no.3
• /
• pp.115-123
• /
• 1980

The rates of escision repair at various doses and times after MNNG treatment in CHO cells were compared with the frequencies of chromosome aberrations to determine a possible relation between there two types of biological phenomena, and the results obtained were as follows: 1. the MNNG-induced excision repair was dose-dependent in te ranges between $0.5 \\times 10^-5$M. The maximum rate of excision repair was occurred in the cells soon after the treatment. The rates were then gradually decreased and appeared about 66% of 0 hour at 24 hours. 2. The rates of chromosome aberrations induced by MNNG was the highest at 6 hours, in which majority were chromatid deletions. The rates of chromatid deletions decreased, whereas chromatid exchanges increased with time, resulting is about equal rates at 24 hours after treatment. 3. The rates of excision repair at different times after MNNG treatment were roughly related to the total breaks per cell. The rates, however, did not show any relation to either chromatid exchanges or deletions. These results may suggest that excision repair may not be directly related to chromosome aberrations in MNNG treated CHO cells.

• BMB Reports
• /
• v.49 no.10
• /
• pp.566-571
• /
• 2016

Forskolin (FSK), an adenylyl cyclase activator, has recently been shown to enhance nucleotide excision repair (NER) upon UV exposure. However, our study revealed that this effect was detected in human skin epithelial ARPE19 cells only in growing cells, but not in non-cycling cells. When the cells were grown at low density (70% confluence), FSK was capable of stimulating cAMP responsive element binding (CREB) phosphorylation, a marker for FSK-stimulated PKA activation, and resulted in a significant increase of NER activity compared to control treatment. However, cells grown under 100% confluent conditions showed neither FSK-induced CREB phosphorylation nor the resulting NER enhancement. These findings indicate that cellular growth is critical for FSK-induced NER enhancement and suggest that cellular growth conditions should be considered as a variable while evaluating a reagent's pharmacotherapeutic efficacy.

• The Korean Journal of Zoology
• /
• v.26 no.3
• /
• pp.171-179
• /
• 1983

Amounts of DNA single strand breaks and unscheduled DNA synthesis in CHO cells exposed to MMS were increased in the presence of 3-aminobenzamide, a potent inhibitor of poly (ADP-ribose) polymerase. However, those in cells irradiated with UV-light were decreased. These results suggest that poly (ADP-ribose) polymerase acts negatively on the MMS-induced base excision repair but positively on the UV-induced nucleotide excision repair. In the combined treatment with MMS and UV-light in the presence of this inhibitor, amounts of strand breaks were just the same as those in the absence of the inhibitor. But those of unscheduled DNA synthesis were increased up to the amount induced by UV-light alone. These results may suggest that poly (ADP-ribose) polymerase affects the incision step of excision repair induced by MMS and UV-light independently, and that it may potentiate the complete cleaving of UV-induced pyrimidine dimers possibly by the repair enzymes which might have been partially inactivated by MMS.

• Clinics in Shoulder and Elbow
• /
• v.21 no.4
• /
• pp.234-239
• /
• 2018

Background: In elbow fracture-dislocation, partial excision of the comminuted radial head fracture that is not amenable to fixation remains controversial considering the accompanying symptoms. This study was undertaken to evaluate the results of radial head partial excision when the comminuted radial head fracture involved <50% of the articular surface in all-arthroscopic repair of elbow fracture-dislocation. Methods: Patients were divided into two groups based on the condition of the radial head fracture. In Group A, the patients had a radial head comminuted fracture involving <50% of the articular surface, and underwent arthroscopic partial excision. Group B was the non-excision group comprising patients with stable and non-displacement fractures. Follow-up consultations were conducted at 6 weeks and at 3, 6, 12, and 24 months after surgery. Results: In all, 19 patients (Group A: 11; Group B: 8) met the inclusion criteria and were enrolled in the study. At the final follow-up, all 19 patients showed complete resolution of elbow instability. No significant differences were observed in the range of motion, visual analogue scale score, and Mayo elbow performance score between groups. Radiological findings did not show any complications of the radiocapitellar joint. However, nonunion of the coracoid fracture was observed in 3 patients (Group A: 1; Group B: 2), without any accompanying instability and clinical symptoms. Conclusions: Considering that the final outcome is coronoid fracture fixation and lateral collateral ligament complex repair for restoring elbow stability, arthroscopic partial excision for radial head comminuted fractures involving <50% of articular surface is an effective and acceptable treatment for elbow fracture-dislocation.

• The Korean Journal of Zoology
• /
• v.20 no.1
• /
• pp.41-48
• /
• 1977

Dose response of DNA repair synthesis induced by bleomycin was dose-dependent in lower doses, and maximum rate of it at 5 $\\mu$g/ml represents about 15% of total cells analyzed. At higher doses DNA-repair synthesis was reduced and the rate of it remained unchanged even prolonged treatment. Pretreatment with BUdR or IUdR was found to enhance DNA repair synthesis and also to interfere with semiconservative DNA synthesis at higher doses. Time dependence study showed that DNA repair synthesis occurred as long as for 24 hours after removal of bleomycin. These results seem to suggest that bleomycin is not to be an effective chemical in inducing excision repair and that damages induced in DNA by this drug might include not only strand breaks but other types of DNA damage.