Genetic susceptibility of newborn daughters to oxidative stress

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Genetic susceptibility of newborn daughters to oxidative stress. / Decordier, Ilse; De Bont, Kelly; De Bock, Kirsten; Mateuca, Raluca; Roelants, Mathieu; Ciardelli, Roberta; Haumont, Dominique; Knudsen, Lisbeth E; Kirsch-Volders, Micheline.

I: Toxicology Letters, Bind 172, Nr. 1-2, 2007, s. 68-84.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Decordier, I, De Bont, K, De Bock, K, Mateuca, R, Roelants, M, Ciardelli, R, Haumont, D, Knudsen, LE & Kirsch-Volders, M 2007, 'Genetic susceptibility of newborn daughters to oxidative stress', Toxicology Letters, bind 172, nr. 1-2, s. 68-84. https://doi.org/10.1016/j.toxlet.2007.05.014

APA

Decordier, I., De Bont, K., De Bock, K., Mateuca, R., Roelants, M., Ciardelli, R., Haumont, D., Knudsen, L. E., & Kirsch-Volders, M. (2007). Genetic susceptibility of newborn daughters to oxidative stress. Toxicology Letters, 172(1-2), 68-84. https://doi.org/10.1016/j.toxlet.2007.05.014

Vancouver

Decordier I, De Bont K, De Bock K, Mateuca R, Roelants M, Ciardelli R o.a. Genetic susceptibility of newborn daughters to oxidative stress. Toxicology Letters. 2007;172(1-2):68-84. https://doi.org/10.1016/j.toxlet.2007.05.014

Author

Decordier, Ilse ; De Bont, Kelly ; De Bock, Kirsten ; Mateuca, Raluca ; Roelants, Mathieu ; Ciardelli, Roberta ; Haumont, Dominique ; Knudsen, Lisbeth E ; Kirsch-Volders, Micheline. / Genetic susceptibility of newborn daughters to oxidative stress. I: Toxicology Letters. 2007 ; Bind 172, Nr. 1-2. s. 68-84.

Bibtex

@article{3ca3ed000b4111df825d000ea68e967b,
title = "Genetic susceptibility of newborn daughters to oxidative stress",
abstract = "A central question in risk assessment is whether newborns' susceptibility to mutagens is different from that of adults. Therefore we investigated whether genotype and/or the DNA strand break repair phenotype in combination with the MN assay would allow estimation of the relative sensitivity of a newborn as compared to his mother for oxidative DNA damage. We compared the in vitro genetic susceptibility for H2O2 in PBMC of 17 mother-newborn daughter pairs taking into account genotypes for relevant DNA repair (hOGG1, XRCC1, XRCC3, XPD) and folate metabolism (MTHFR) polymorphisms. After in vitro challenge with H2O2 the repair capacity was assessed by the Comet assay and chromosome/genome mutations by the cytokinesis-block MN assay. No statistically significant differences were found between mothers and their newborn daughters either for initial DNA damage or for residual DNA damage. Mothers showed higher background frequencies of MN as compared to their newborn daughters, due to the age factor. This was confirmed by significantly higher frequencies of MN observed in mothers versus newborn daughters for several genotypes. No genotype with a significant effect on DNA repair capacity in newborns was identified. Concerning MN frequencies, however, newborns carrying the variant XRCC3(241) genotype might be at higher risk for the induction of MN by oxidative stress. Multivariate analysis revealed a significant protective effect of maternal antioxidant supplementation during pregnancy against oxidative DNA damage in newborns in terms of MN frequencies. However, these conclusions might not be extrapolable to other types of DNA damage and need confirmation in a study on a larger population.",
author = "Ilse Decordier and {De Bont}, Kelly and {De Bock}, Kirsten and Raluca Mateuca and Mathieu Roelants and Roberta Ciardelli and Dominique Haumont and Knudsen, {Lisbeth E} and Micheline Kirsch-Volders",
note = "Keywords: Adult; Antioxidants; Cells, Cultured; DNA Damage; DNA Glycosylases; DNA-Binding Proteins; Female; Genotype; Humans; Hydrogen Peroxide; Infant, Newborn; Leukocytes, Mononuclear; Methylenetetrahydrofolate Reductase (NADPH2); Micronucleus Tests; Mutagens; Oxidative Stress; Phenotype; Pilot Projects; Polymorphism, Genetic; Pregnancy; Risk Assessment; Risk Factors; Xeroderma Pigmentosum Group D Protein",
year = "2007",
doi = "10.1016/j.toxlet.2007.05.014",
language = "English",
volume = "172",
pages = "68--84",
journal = "Toxicology Letters",
issn = "0378-4274",
publisher = "Elsevier Ireland Ltd",
number = "1-2",

}

RIS

TY - JOUR

T1 - Genetic susceptibility of newborn daughters to oxidative stress

AU - Decordier, Ilse

AU - De Bont, Kelly

AU - De Bock, Kirsten

AU - Mateuca, Raluca

AU - Roelants, Mathieu

AU - Ciardelli, Roberta

AU - Haumont, Dominique

AU - Knudsen, Lisbeth E

AU - Kirsch-Volders, Micheline

N1 - Keywords: Adult; Antioxidants; Cells, Cultured; DNA Damage; DNA Glycosylases; DNA-Binding Proteins; Female; Genotype; Humans; Hydrogen Peroxide; Infant, Newborn; Leukocytes, Mononuclear; Methylenetetrahydrofolate Reductase (NADPH2); Micronucleus Tests; Mutagens; Oxidative Stress; Phenotype; Pilot Projects; Polymorphism, Genetic; Pregnancy; Risk Assessment; Risk Factors; Xeroderma Pigmentosum Group D Protein

PY - 2007

Y1 - 2007

N2 - A central question in risk assessment is whether newborns' susceptibility to mutagens is different from that of adults. Therefore we investigated whether genotype and/or the DNA strand break repair phenotype in combination with the MN assay would allow estimation of the relative sensitivity of a newborn as compared to his mother for oxidative DNA damage. We compared the in vitro genetic susceptibility for H2O2 in PBMC of 17 mother-newborn daughter pairs taking into account genotypes for relevant DNA repair (hOGG1, XRCC1, XRCC3, XPD) and folate metabolism (MTHFR) polymorphisms. After in vitro challenge with H2O2 the repair capacity was assessed by the Comet assay and chromosome/genome mutations by the cytokinesis-block MN assay. No statistically significant differences were found between mothers and their newborn daughters either for initial DNA damage or for residual DNA damage. Mothers showed higher background frequencies of MN as compared to their newborn daughters, due to the age factor. This was confirmed by significantly higher frequencies of MN observed in mothers versus newborn daughters for several genotypes. No genotype with a significant effect on DNA repair capacity in newborns was identified. Concerning MN frequencies, however, newborns carrying the variant XRCC3(241) genotype might be at higher risk for the induction of MN by oxidative stress. Multivariate analysis revealed a significant protective effect of maternal antioxidant supplementation during pregnancy against oxidative DNA damage in newborns in terms of MN frequencies. However, these conclusions might not be extrapolable to other types of DNA damage and need confirmation in a study on a larger population.

AB - A central question in risk assessment is whether newborns' susceptibility to mutagens is different from that of adults. Therefore we investigated whether genotype and/or the DNA strand break repair phenotype in combination with the MN assay would allow estimation of the relative sensitivity of a newborn as compared to his mother for oxidative DNA damage. We compared the in vitro genetic susceptibility for H2O2 in PBMC of 17 mother-newborn daughter pairs taking into account genotypes for relevant DNA repair (hOGG1, XRCC1, XRCC3, XPD) and folate metabolism (MTHFR) polymorphisms. After in vitro challenge with H2O2 the repair capacity was assessed by the Comet assay and chromosome/genome mutations by the cytokinesis-block MN assay. No statistically significant differences were found between mothers and their newborn daughters either for initial DNA damage or for residual DNA damage. Mothers showed higher background frequencies of MN as compared to their newborn daughters, due to the age factor. This was confirmed by significantly higher frequencies of MN observed in mothers versus newborn daughters for several genotypes. No genotype with a significant effect on DNA repair capacity in newborns was identified. Concerning MN frequencies, however, newborns carrying the variant XRCC3(241) genotype might be at higher risk for the induction of MN by oxidative stress. Multivariate analysis revealed a significant protective effect of maternal antioxidant supplementation during pregnancy against oxidative DNA damage in newborns in terms of MN frequencies. However, these conclusions might not be extrapolable to other types of DNA damage and need confirmation in a study on a larger population.

U2 - 10.1016/j.toxlet.2007.05.014

DO - 10.1016/j.toxlet.2007.05.014

M3 - Journal article

C2 - 17614221

VL - 172

SP - 68

EP - 84

JO - Toxicology Letters

JF - Toxicology Letters

SN - 0378-4274

IS - 1-2

ER -

ID: 17264879