• Journal of Genetic Medicine
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• v.2 no.1
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• pp.31-34
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• 1998

The N-methylpurine-DNA glycosylase (MPG), a ubiquitous DNA repair enzyme, removes N-methylpurine and other damaged purines induced in DNA. Tissue-specific mRNA levels of the N-methylpurine-DNA glycosylase (MPG) were investigated in Balb/c mice of four different growing stages; newborn, 1, 4 and 8-weeks postpartum. MPG expressions in the newborn and the 8-week-old mice were the highest in thymus and testis, respectively. The tested tissues of the newborn mice had consistently higher MPG mRNA level than 8-week-old adults except in testis and thymus. The MPG mRNA level in testis was the lowest in the newborn mice, but it attained the highest in the 8-week-old mice. The levels of MPG mRNA among the different tissues in the newborn and the 8-week-old mice were more than 9.0 and 19.0-fold respectively. These results suggest that the of MPG expression was dependent on the growing stage and had tissue-specificity.

• Environmental Mutagens and Carcinogens
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• v.10 no.1
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• pp.1-10
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• 1990

The regulation of DNA repair genes expression was investigated using fused genes, in which the promoter of repair genes was hybridized with the lacZ structural gene. The activities of beta-galactosidase expressed from the fused gense were highly increased when the host cells were exposed to methylating agents, such as methyl methansulfonate (MMS), N-methyl-N'-nitro-nitrosoguanidine (MNNG) and methyl nitrosourea (MNU). On the other hand, the enzyme activities from the fused genes were not induced when the cells were treated with ethylating or nonalkylating agents, such as ethyl methansulfonate (EMS), 4-nitroquinoline-1-oxide (4NQO), Bleomycin, and Benzo(a)pyrene (BP).

• Toxicological Research
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• v.7 no.2
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• pp.157-163
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• 1991

The effect of patulin, a mycotoxin, on the growth of Escherichia coli cell was investigated. E. coli cell elongation usually shown in SOS-response for DNA repair was induced by 20 mg of patulin per ml. After staining the E. coli chromosome with fluorescence dye(DAPI, 4', 6-diamino-2-phenyl-indole), chromosomal DNA partitioning was not affected by patulin. The observation indicateds that patulin acts as a DNA damaging agent which is effective for E. coli cell elongation introduced by the inhibition of septum formation.

• Molecular & Cellular Toxicology
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• v.4 no.1
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• pp.66-71
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• 2008

Long term exposure of Jurkat cells to 2 ATA pressure resulted in the inhibition of cell growth. Under a 2 ATA pressure, the morphological changes in the cells were visualized by electron microscopy. The cells exhibited significant inhibitory responses after three passages. However, short-term exposure study was carried out, 2 ATA pressure may have beneficial effects. The Jurkat cells were exposed to $H_2O_2$ (25 and $50{\mu}M$) in order to induce DNA damage, and then incubated under at either normal pressure or 2 ATA for 1 or 2 hours in order to recover the DNA damage. The extent of DNA damage was determined via Comet assay. More recovery from DNA damage was observed at 2 ATA than at normal pressure. The activity of the DNA repair enzymes, DNA polymerase-$\beta$, was also evaluated at both normal pressure and 2 ATA. The activity of DNA polymerase-$\beta$ was observed to have increased significantly at the 2 ATA than at normal pressure. In conclusion, the effects of hyperbaric pressure from 1 ATA to 2 ATA on biochemical systems can be either beneficial or harmful. Long term exposure to hyperbaric pressure clearly inhibited cell proliferation and caused genotoxic effects, but short-term exposure to hyperbaric pressure proved to be beneficial in terms of bolstering the DNA repair system. The results of the present study have clinical therapeutic application, and might prove to be an useful tool in the study of genotoxicity in the future.

• BMB Reports
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• v.30 no.1
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• pp.66-72
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• 1997

A mammalian DNA repair enzyme, UV endonuclease III which also functions as a ribosomal protein S3 (rpS3), was purified from mouse cells and characterized. UV endonuclease III was previously cloned and known to yield a peptide of 32 kDa upon expression in E. coli [Kim et al., (1995) J. Bioi. Chem. 270, 13620-13629]. However, biochemically purified UV endonuclease III, which has a sedimentation coefficient of 3.25, appears to have an additional peptide of 28 kDa. It appears that two bands were derived from one complex, judging from the comparison of the nuclease activity on the native and SDS-gel electrophoreses. UV endonuclease III becomes non-specific upon purification and this phenomenon is more significant in the case of pure fractions of the enzyme. Non-specific activity was not influenced by pH or any salt conditions.

• IMMUNE NETWORK
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• v.2 no.4
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• pp.208-216
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• 2002

Background: Reactive oxygen and nitrogen are produced by rheumatoid arthritis (RA) synovial tissue and can induce mutations in key genes. Normally, this process is prevented by a DNA mismatch repair (MMR) system that maintains sequence fidelity. Key members of the MMR system include MutS${\alpha}$ (comprised of hMSH2 and hMSH6), which can sense and repair single base mismatches and 8-oxoguanine, and MutS${\beta}$ (comprised of hMSH2 and hMSH3), which repairs longer insertion/deletion loops. Methods: To provide further evidence of DNA damage, we analyzed synovial tissues for microsatellite instability (MSI). MSI was examined by PCR on genomic DNA of paired synovial tissue and peripheral blood cells (PBC) of RA patients using specific primer sequences for 5 key microsatellites. Results: Surprisingly, abundant MSI was observed in RA synovium compared with osteoarthritis (OA) tissue. Western blot analysis of the same tissues for the expression of MMR proteins demonstrated decreased hMSH6 and increased hMSH3 in RA synovium. To evaluate potential mechanisms of MMR regulation in arthritis, fibroblast-like synoviocytes (FLS) were isolated from synovial tissues and incubated with the nitric oxide donor S-nitroso-N-acetylpenicillamine (SNAP). Western blot analysis demonstrated constitutive expression of hMSH2, 3 and 6 in RA and OA FLS. When FLS were cultured with SNAP, the RA synovial pattern of MMR expression was reproduced (high hMSH3, low hMSH6). Conclusion: Therefore, oxidative stress can relax the DNA MMR system in RA by suppressing hMSH6. Decreased hMSH6 can subsequently interfere with repair of single base mutations, which is the type observed in RA. We propose that oxidative stress not only creates DNA adducts that are potentially mutagenic, but also suppresses the mechanisms that limit the DNA damage.

• Animal cells and systems
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• v.1 no.3
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• pp.451-455
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• 1997

The effects of nalidixic acid, mitomycin C, and cadmium chloride $(CdCI_2)$ on the activity of 8-hydroxyguanine $(oh^8Gua)$ endonuclease, a DNA repair enzyme for oxidatively modified guanine, $(oh^8Gua$ were studied. Nalidixic acid and mitomycin C, typical inducers of the S0S DNA repair response in E. coli, showed different effects. Nalidixic acid raised the activity of this enzyme, but mitomycin C did not show such an effect. Cadmium chloride also induced the enzyme activity, These results show that the expression of $oh^8$ Gua endonuclease is regulated by multiple factors and can be induced under stressful conditions. In an attempt to demonstrate the importance of this enzyme in defense against DNA damage and mutagenesis, we also characterized mutM mutant for its oh8 Gua endonuclease activity. The mutM mutant showed no detectable $oh^8$ Gua endonuclease activity, unlike its wild type showing high activity. In addition, paraquat, a superoxide producing compound, failed to elevate $oh^8Gua$ endonuclease activity in this mutant. These results suggest that the mutM gene is identical to the $oh^8Gua$ endonuclease gene of E. coli. Taken together with previous reports, these results suggest that $oh^8Gua$ endonuclease plays a crucial role in the protection of aerobically growing organisms from threats of oxidative DNA damage and mutation.

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.126-126
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• 2003

Welding fume (WF) induces pulmonary disease including pneumoconiosis. To investigate whether reactive oxygen species-induced oxidative DNA damage occurs during welding fume exposure and the upregulation of DNA repair mechanisms is accompanied, SPF SD rats were exposed to welding fumes with the concentrations of 65.6${\pm}$2.9 mg/㎥(low dose) and 116.8${\pm}$3.9 mg/㎥ (high dose) of total suspended particulate for 2 hrs per day in an inhalation chamber for a total of 2hrs, 15 or 30 days.(omitted)

• Proceedings of the Korean Society of Applied Pharmacology
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• 1995.04a
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• pp.80-80
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• 1995

T4 Endonuclease V (Mw 16,000) acts as a repair enzyme for UV induced pyrimidine dimers in DNA. Many researchers have studied the biochemical characteristics of the enzyme. However the precise action mechanism of T4 endo V has not fully elucidated yet. In our laboratory NMR spectroscopy technique is being used for the structural study of T4 endo V. Because of its low temperature stability and high content of ${\alpha}$-helix, the conventional $^1$H NMR technique was inapplicable. Therefore we utilized stable isotope labeling technique and so far prepared about 10 amino acid specific labeled proteins. The HSQC spectra of amino acid specific labeled proteins will help us to interpret the triple resonance 3D, 4D data which are under processing, We also studied the behaviors of specific amino acid residues whose roles might be critical. When the enzyme labeled by $\^$15/N-Thr was mixed with the substrate oligonucleotide (semispecific -TT- sequence), one crosspeak in its HSQC spectrum was completely desappeared, which means that one of seven Thr residues is in the binding site of the enzyme with DNA, This result is well consistent with previous report that implicated the Thr 2 residue in the activity of the enzyme. Similar studies were carried on the behaviors of Arg and Tyr residues.

• The Korean Journal of Food And Nutrition
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• v.33 no.3
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• pp.309-316
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• 2020

In this study, we investigated the protective effects of Ulva lactuca methanol extracts against ultraviolet B (UVB)-induced DNA damage in HaCaT cells. First, the contents of general and antioxidative nutrient contents of Ulva lactuca were measured. The moisture, carbohydrate, crude protein, crude fat and ash were 14.01%, 44.80%, 23.19%, 3.10% and 14.90%, respectively. Magnesium that acts as DNA repair enzyme cofactor was the most abundant mineral followed by Ca, P and Fe. The total phenolic and anthocyanoside contents of Ulva lactuca were 2.69 mg/g and 0.13 mg/g, respectively. Cells treated with Ulva lactuca methanol extracts for 24 hours post UVB exposure increased cell viability in a concentration-dependent manner compared to the non-treated control. Also, Ulva lactuca methanol extracts decreased the levels of UVB-induced DNA damage such as cyclobutane pyrimidine dimer and DNA damage response (DDR) proteins such as p-p53 and p21. These results suggest that Ulva lactuca methanol extracts comprising physiological active substances such as Mg, polyphenols and anthocyanosides promote DNA repair by regulating genes related with DDR.