Enhancement of methyl methanesulfonate-induced base excision repair in the presence of selenomethionine on p53-dependent pathway

Hwa Jin Jung, Ju Han Lee, Young R. Seo

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Selenomethionine (SeMet) has been identified as a chemopreventive antioxidant to activate p53-mediated nucleotide excision repair. In this study, we examined whether p53-mediated base excision repair (BER) might be induced by SeMet. When methyl methanesulfonate, a BER-inducing agent, was treated in the cells, DNA damage was rapidly decreased in the presence of SeMet. In addition, our data showed that the removal of apurinic/apyrimidinic sites was significantly enhanced in the presence of SeMet. Furthermore, we observed that the expression of gadd45a, known to involve BER as one of the p53 downstream genes, was increased by SeMet in p53 wild-type RKO cells. Those results supported the proposal that BER activity might be dependent on wild-type p53 under the modulation of gadd45a expression in response to SeMet. We suggested that p53-dependent BER activity as a distinct mechanism of SeMet might play an important role to prevent cancer caused by various oxidative stresses.

Original languageEnglish (US)
Pages (from-to)340-344
Number of pages5
JournalJournal of Medicinal Food
Volume12
Issue number2
DOIs
StatePublished - Apr 1 2009
Externally publishedYes

Fingerprint

Selenomethionine
Methyl Methanesulfonate
DNA Repair
p53 Genes
DNA Damage
Oxidative Stress
Antioxidants

Keywords

  • Base excision repair
  • Chemoprevention
  • P53
  • Selenium

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Nutrition and Dietetics

Cite this

Enhancement of methyl methanesulfonate-induced base excision repair in the presence of selenomethionine on p53-dependent pathway. / Jung, Hwa Jin; Lee, Ju Han; Seo, Young R.

In: Journal of Medicinal Food, Vol. 12, No. 2, 01.04.2009, p. 340-344.

Research output: Contribution to journalArticle

@article{b4caaec6bf5240b392808d602c366297,
title = "Enhancement of methyl methanesulfonate-induced base excision repair in the presence of selenomethionine on p53-dependent pathway",
abstract = "Selenomethionine (SeMet) has been identified as a chemopreventive antioxidant to activate p53-mediated nucleotide excision repair. In this study, we examined whether p53-mediated base excision repair (BER) might be induced by SeMet. When methyl methanesulfonate, a BER-inducing agent, was treated in the cells, DNA damage was rapidly decreased in the presence of SeMet. In addition, our data showed that the removal of apurinic/apyrimidinic sites was significantly enhanced in the presence of SeMet. Furthermore, we observed that the expression of gadd45a, known to involve BER as one of the p53 downstream genes, was increased by SeMet in p53 wild-type RKO cells. Those results supported the proposal that BER activity might be dependent on wild-type p53 under the modulation of gadd45a expression in response to SeMet. We suggested that p53-dependent BER activity as a distinct mechanism of SeMet might play an important role to prevent cancer caused by various oxidative stresses.",
keywords = "Base excision repair, Chemoprevention, P53, Selenium",
author = "Jung, {Hwa Jin} and Lee, {Ju Han} and Seo, {Young R.}",
year = "2009",
month = "4",
day = "1",
doi = "10.1089/jmf.2007.0709",
language = "English (US)",
volume = "12",
pages = "340--344",
journal = "Journal of Medicinal Food",
issn = "1096-620X",
publisher = "Mary Ann Liebert Inc.",
number = "2",

}

TY - JOUR

T1 - Enhancement of methyl methanesulfonate-induced base excision repair in the presence of selenomethionine on p53-dependent pathway

AU - Jung, Hwa Jin

AU - Lee, Ju Han

AU - Seo, Young R.

PY - 2009/4/1

Y1 - 2009/4/1

N2 - Selenomethionine (SeMet) has been identified as a chemopreventive antioxidant to activate p53-mediated nucleotide excision repair. In this study, we examined whether p53-mediated base excision repair (BER) might be induced by SeMet. When methyl methanesulfonate, a BER-inducing agent, was treated in the cells, DNA damage was rapidly decreased in the presence of SeMet. In addition, our data showed that the removal of apurinic/apyrimidinic sites was significantly enhanced in the presence of SeMet. Furthermore, we observed that the expression of gadd45a, known to involve BER as one of the p53 downstream genes, was increased by SeMet in p53 wild-type RKO cells. Those results supported the proposal that BER activity might be dependent on wild-type p53 under the modulation of gadd45a expression in response to SeMet. We suggested that p53-dependent BER activity as a distinct mechanism of SeMet might play an important role to prevent cancer caused by various oxidative stresses.

AB - Selenomethionine (SeMet) has been identified as a chemopreventive antioxidant to activate p53-mediated nucleotide excision repair. In this study, we examined whether p53-mediated base excision repair (BER) might be induced by SeMet. When methyl methanesulfonate, a BER-inducing agent, was treated in the cells, DNA damage was rapidly decreased in the presence of SeMet. In addition, our data showed that the removal of apurinic/apyrimidinic sites was significantly enhanced in the presence of SeMet. Furthermore, we observed that the expression of gadd45a, known to involve BER as one of the p53 downstream genes, was increased by SeMet in p53 wild-type RKO cells. Those results supported the proposal that BER activity might be dependent on wild-type p53 under the modulation of gadd45a expression in response to SeMet. We suggested that p53-dependent BER activity as a distinct mechanism of SeMet might play an important role to prevent cancer caused by various oxidative stresses.

KW - Base excision repair

KW - Chemoprevention

KW - P53

KW - Selenium

UR - http://www.scopus.com/inward/record.url?scp=67649540487&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=67649540487&partnerID=8YFLogxK

U2 - 10.1089/jmf.2007.0709

DO - 10.1089/jmf.2007.0709

M3 - Article

C2 - 19459735

AN - SCOPUS:67649540487

VL - 12

SP - 340

EP - 344

JO - Journal of Medicinal Food

JF - Journal of Medicinal Food

SN - 1096-620X

IS - 2

ER -