An endonuclease activity in human polymorphonuclear neutrophils that removes 8-hydroxyguanine residues from DNA

Chung, Myung‐Hee; Kim, Hun-Sik; Ohtsuka, Eiko; Kasai, Hiroshi; Yamamoto, Fukuju; Nishimura, Susumu

doi:10.1016/0006-291x(91)91059-l

Cited by 78 publications

(26 citation statements)

References 8 publications

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“…A mammalian counterpart of the fpg gene has not yet been cloned, although several reports support the presence of DNA glycosylases that remove 8-oxoG in mammalian cells [217][218][219]. It is, however, less clear what fraction of the repair is caused by MPG, which removes 8-oxoG in addition to a wide range of alkylated purines [130,145,146].…”

Section: Fpg Family and The Oxog Systemmentioning

confidence: 99%

DNA glycosylases in the base excision repair of DNA

Krokan

Standal

Slupphaug

1997

Biochemical Journal

771

566

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A wide range of cytotoxic and mutagenic DNA bases are removed by different DNA glycosylases, which initiate the base excision repair pathway. DNA glycosylases cleave the Nglycosylic bond between the target base and deoxyribose, thus releasing a free base and leaving an apurinic\apyrimidinic (AP) site. In addition, several DNA glycosylases are bifunctional, since they also display a lyase activity that cleaves the phosphodiester backbone 3h to the AP site generated by the glycosylase activity. Structural data and sequence comparisons have identified common features among many of the DNA glycosylases. Their active sites have a structure that can only bind extrahelical target bases, as observed in the crystal structure of human uracil-DNA glycosylase in a complex with double-stranded DNA. Nucleotide flipping is apparently actively facilitated by the enzyme. With bacteriophage T4 endonuclease V, a pyrimidine-

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Section: Fpg Family and The Oxog Systemmentioning

confidence: 99%

DNA glycosylases in the base excision repair of DNA

Krokan

Standal

Slupphaug

1997

Biochemical Journal

771

566

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“…It has been clear that a significant inflammatory response including up-regulation of the inducible nitric oxide synthase (iNOS) occurs during the first hour after the injury, and iNOS-mediated NO production is profoundly up-regulated (Chung et al 1991). NO has important effects on cellular respiration and mitochondrial ROS production, which could either contribute or exacerbate cellular damage (Rhee et al 1998).…”

Section: Discussionmentioning

confidence: 99%

Neuroendocrine System Response Modulates Oxidative Cellular Damage in Burn Patients

Xie

Shinozawa

Sasaki

et al. 2007

Tohoku J. Exp. Med.

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Oxygen-derived free radicals play important roles in pathophysiological processes in critically ill patients, but the data characterizing relationships between radicals and neuroendocrine system response are sparse. To search the cue to reduce the oxidative cellular damage from the point of view of neuroendocrine system response, we studied the indicators of neuroendocrine and inflammatory responses excreted in urine in 14 burn patients (42.3 ± 31.4 years old, and 32.3 ± 27.6% burn of total body surface area [%TBSA]) during the first seven days post burn. The daily mean amounts of urinary excretion of 8-hydroxy-2′-deoxy-guanosine (8-OHdG), a marker of oxidative cellular damage, were above the upper limit of the standard value during the studied period. The total amount of urinary excretion of 8-OHdG in the first day post burn correlated with burn severity indices: %TBSA (r = 0.63, p = 0.021) and burn index (r = 0.70, p = 0.008). The daily urinary excretion of 8-OHdG correlated with the daily urinary excretion of norepinephrine and nitrite plus nitrate (NOx) during the studied period except day 2 post burn, and correlated with the daily urinary excretion of 17-hydroxycorticosteriod (17-OHCS) in days 2, 3, and 7 post burn. These data suggest that oxidative cellular damage correlates with burn severity and neuroendocrine system response modulates inflammation and oxidative cellular damage. Modulation of neuroendocrine system response and inflammation in the treatment in the early phase of burn may be useful to reduce the oxidative cellular damage and to prevent multiple organ failures in patients with extensive burn. free radical; 8-OHdG; norepinephrine; 17-OHCS; nitrogen oxide

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“…The cell extracts were prepared as described previously with slight modification (Chung et al, 1991). At the indicated times, HL-60 cells were washed three times with cold PBS.…”

Section: Preparation Of Cell Extract For the Dna Nicking Assaymentioning

confidence: 99%

“…The DNA nicking assay was done as described previously (Chung et al, 1991). Reaction mixtures (100 µl) containing 0.4 pmol of labeled 21-mer duplex substrate DNA, 50 µg proteins of the cell extract or 2 µg of rhOGG1, 2% glycerol in buffer B were incubated at 37 o C for 1 h. Reactions were stopped by adding 200 µl of tRNA solution (1 mg/ml tRNA, 0.45 M sodium acetate, pH 5.2) and 200 µl of phenol: chloroform (1:1, v/v).…”

Section: Assay Of Dna Nicking Activitymentioning

confidence: 99%

Expression of hOGG1 protein during differentiation of HL-60 cells

Lee

Lee²,

Chung³

2003

Exp Mol Med

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Human 8-oxo-G-DNA glycosylase 1 (hOGG1) is a DNA glycosylase to cleave 8-oxo-7,8-dihydroguanine (8-oxo-G), a mutagenic DNA adduct formed by oxidant stresses. Here, we examined hOGG1 protein expression and repair activity to nick a DNA strand at the site of 8-oxo-G during differentiation of hematopoietic cells using HL-60 cells. Overall expression of hOGG1 protein was increased during granulocytic differentiation of HL-60 cells induced by DMSO and monocytic differentiation by vitamine D 3 . Greater level of hOGG1 protein was expressed in DMSO-treated cells. However, change in the DNA nicking activity was not in parallel with the change in hOGG1 protein expression, especially in PMA-treated cells. In PMAtreated cells, the level of hOGG1 protein was lowered, even though the DNA nicking activity was elevated, in a manner similar to the changes in serumdeprived HL-60 cells. These results indicate that hOGG1 expression change during differentiation of hematopoietic stem cells for adaptation to new environments. And the DNA cleaving activity may require additional factor(s) other than expressed hOGG1 protein, especially in apoptotic cell death.

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An endonuclease activity in human polymorphonuclear neutrophils that removes 8-hydroxyguanine residues from DNA

Cited by 78 publications

References 8 publications

DNA glycosylases in the base excision repair of DNA

DNA glycosylases in the base excision repair of DNA

Neuroendocrine System Response Modulates Oxidative Cellular Damage in Burn Patients

Expression of hOGG1 protein during differentiation of HL-60 cells

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