Hydrogen peroxide induced genomic instability in nucleotide excision repair-deficient lymphoblastoid cells
Background The Nucleotide Excision Repair (NER) pathway specialises in UV-induced DNA damage repair. Inherited defects in the NER can predispose individuals to Xeroderma Pigmentosum (XP). UV-induced DNA damage cannot account for the manifestation of XP in organ systems not directly exposed to sunlig...
Ausführliche Beschreibung
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| Autor*in: |
Gopalakrishnan, Kalpana [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2010 |
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| Anmerkung: |
© Gopalakrishnan et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (<url>http://creativecommons.org/licenses/by/2.0</url>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
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| Übergeordnetes Werk: |
Enthalten in: Genome integrity - Cham, Switzerland : Springer International Publishing AG, 2010, 1(2010), 1 vom: 22. Dez. |
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| Übergeordnetes Werk: |
volume:1 ; year:2010 ; number:1 ; day:22 ; month:12 |
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| DOI / URN: |
10.1186/2041-9414-1-16 |
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| Katalog-ID: |
SPR030900220 |
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| 520 | |a Background The Nucleotide Excision Repair (NER) pathway specialises in UV-induced DNA damage repair. Inherited defects in the NER can predispose individuals to Xeroderma Pigmentosum (XP). UV-induced DNA damage cannot account for the manifestation of XP in organ systems not directly exposed to sunlight. While the NER has recently been implicated in the repair of oxidative DNA lesions, it is not well characterised. Therefore we sought to investigate the role of NER factors Xeroderma Pigmentosum A (XPA), XPB and XPD in oxidative DNA damage-repair by subjecting lymphoblastoid cells from patients suffering from XP-A, XP-D and XP-B with Cockayne Syndrome to hydrogen peroxide ($ H_{2} %$ O_{2} $). Results Loss of functional XPB or XPD but not XPA led to enhanced sensitivity towards $ H_{2} %$ O_{2} $-induced cell death. XP-deficient lymphoblastoid cells exhibited increased susceptibility to $ H_{2} %$ O_{2} $-induced DNA damage with XPD showing the highest susceptibility and lowest repair capacity. Furthermore, XPB- and XPD-deficient lymphoblastoid cells displayed enhanced DNA damage at the telomeres. XPA- and XPB-deficient lymphoblastoid cells also showed differential regulation of XPD following $ H_{2} %$ O_{2} $ treatment. Conclusions Taken together, our data implicate a role for the NER in $ H_{2} %$ O_{2} $-induced oxidative stress management and further corroborates that oxidative stress is a significant contributing factor in XP symptoms. Resistance of XPA-deficient lymphoblastoid cells to $ H_{2} %$ O_{2} $-induced cell death while harbouring DNA damage poses a potential cancer risk factor for XPA patients. Our data implicate XPB and XPD in the protection against oxidative stress-induced DNA damage and telomere shortening, and thus premature senescence. | ||
| 650 | 4 | |a Nucleotide Excision Repair |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Base Excision Repair |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Xeroderma Pigmentosum |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Tail Moment |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Cockayne Syndrome |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Low, Grace Kah Mun |4 aut | |
| 700 | 1 | |a Ting, Aloysius Poh Leong |4 aut | |
| 700 | 1 | |a Srikanth, Prarthana |4 aut | |
| 700 | 1 | |a Slijepcevic, Predrag |4 aut | |
| 700 | 1 | |a Hande, M Prakash |4 aut | |
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10.1186/2041-9414-1-16 doi (DE-627)SPR030900220 (SPR)2041-9414-1-16-e DE-627 ger DE-627 rakwb eng Gopalakrishnan, Kalpana verfasserin aut Hydrogen peroxide induced genomic instability in nucleotide excision repair-deficient lymphoblastoid cells 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Gopalakrishnan et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (<url>http://creativecommons.org/licenses/by/2.0</url>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background The Nucleotide Excision Repair (NER) pathway specialises in UV-induced DNA damage repair. Inherited defects in the NER can predispose individuals to Xeroderma Pigmentosum (XP). UV-induced DNA damage cannot account for the manifestation of XP in organ systems not directly exposed to sunlight. While the NER has recently been implicated in the repair of oxidative DNA lesions, it is not well characterised. Therefore we sought to investigate the role of NER factors Xeroderma Pigmentosum A (XPA), XPB and XPD in oxidative DNA damage-repair by subjecting lymphoblastoid cells from patients suffering from XP-A, XP-D and XP-B with Cockayne Syndrome to hydrogen peroxide ($ H_{2} %$ O_{2} $). Results Loss of functional XPB or XPD but not XPA led to enhanced sensitivity towards $ H_{2} %$ O_{2} $-induced cell death. XP-deficient lymphoblastoid cells exhibited increased susceptibility to $ H_{2} %$ O_{2} $-induced DNA damage with XPD showing the highest susceptibility and lowest repair capacity. Furthermore, XPB- and XPD-deficient lymphoblastoid cells displayed enhanced DNA damage at the telomeres. XPA- and XPB-deficient lymphoblastoid cells also showed differential regulation of XPD following $ H_{2} %$ O_{2} $ treatment. Conclusions Taken together, our data implicate a role for the NER in $ H_{2} %$ O_{2} $-induced oxidative stress management and further corroborates that oxidative stress is a significant contributing factor in XP symptoms. Resistance of XPA-deficient lymphoblastoid cells to $ H_{2} %$ O_{2} $-induced cell death while harbouring DNA damage poses a potential cancer risk factor for XPA patients. Our data implicate XPB and XPD in the protection against oxidative stress-induced DNA damage and telomere shortening, and thus premature senescence. Nucleotide Excision Repair (dpeaa)DE-He213 Base Excision Repair (dpeaa)DE-He213 Xeroderma Pigmentosum (dpeaa)DE-He213 Tail Moment (dpeaa)DE-He213 Cockayne Syndrome (dpeaa)DE-He213 Low, Grace Kah Mun aut Ting, Aloysius Poh Leong aut Srikanth, Prarthana aut Slijepcevic, Predrag aut Hande, M Prakash aut Enthalten in Genome integrity Cham, Switzerland : Springer International Publishing AG, 2010 1(2010), 1 vom: 22. Dez. (DE-627)627611745 (DE-600)2556795-0 2041-9414 nnns volume:1 year:2010 number:1 day:22 month:12 https://dx.doi.org/10.1186/2041-9414-1-16 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 1 2010 1 22 12 |
| spelling |
10.1186/2041-9414-1-16 doi (DE-627)SPR030900220 (SPR)2041-9414-1-16-e DE-627 ger DE-627 rakwb eng Gopalakrishnan, Kalpana verfasserin aut Hydrogen peroxide induced genomic instability in nucleotide excision repair-deficient lymphoblastoid cells 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Gopalakrishnan et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (<url>http://creativecommons.org/licenses/by/2.0</url>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background The Nucleotide Excision Repair (NER) pathway specialises in UV-induced DNA damage repair. Inherited defects in the NER can predispose individuals to Xeroderma Pigmentosum (XP). UV-induced DNA damage cannot account for the manifestation of XP in organ systems not directly exposed to sunlight. While the NER has recently been implicated in the repair of oxidative DNA lesions, it is not well characterised. Therefore we sought to investigate the role of NER factors Xeroderma Pigmentosum A (XPA), XPB and XPD in oxidative DNA damage-repair by subjecting lymphoblastoid cells from patients suffering from XP-A, XP-D and XP-B with Cockayne Syndrome to hydrogen peroxide ($ H_{2} %$ O_{2} $). Results Loss of functional XPB or XPD but not XPA led to enhanced sensitivity towards $ H_{2} %$ O_{2} $-induced cell death. XP-deficient lymphoblastoid cells exhibited increased susceptibility to $ H_{2} %$ O_{2} $-induced DNA damage with XPD showing the highest susceptibility and lowest repair capacity. Furthermore, XPB- and XPD-deficient lymphoblastoid cells displayed enhanced DNA damage at the telomeres. XPA- and XPB-deficient lymphoblastoid cells also showed differential regulation of XPD following $ H_{2} %$ O_{2} $ treatment. Conclusions Taken together, our data implicate a role for the NER in $ H_{2} %$ O_{2} $-induced oxidative stress management and further corroborates that oxidative stress is a significant contributing factor in XP symptoms. Resistance of XPA-deficient lymphoblastoid cells to $ H_{2} %$ O_{2} $-induced cell death while harbouring DNA damage poses a potential cancer risk factor for XPA patients. Our data implicate XPB and XPD in the protection against oxidative stress-induced DNA damage and telomere shortening, and thus premature senescence. Nucleotide Excision Repair (dpeaa)DE-He213 Base Excision Repair (dpeaa)DE-He213 Xeroderma Pigmentosum (dpeaa)DE-He213 Tail Moment (dpeaa)DE-He213 Cockayne Syndrome (dpeaa)DE-He213 Low, Grace Kah Mun aut Ting, Aloysius Poh Leong aut Srikanth, Prarthana aut Slijepcevic, Predrag aut Hande, M Prakash aut Enthalten in Genome integrity Cham, Switzerland : Springer International Publishing AG, 2010 1(2010), 1 vom: 22. Dez. (DE-627)627611745 (DE-600)2556795-0 2041-9414 nnns volume:1 year:2010 number:1 day:22 month:12 https://dx.doi.org/10.1186/2041-9414-1-16 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 1 2010 1 22 12 |
| allfields_unstemmed |
10.1186/2041-9414-1-16 doi (DE-627)SPR030900220 (SPR)2041-9414-1-16-e DE-627 ger DE-627 rakwb eng Gopalakrishnan, Kalpana verfasserin aut Hydrogen peroxide induced genomic instability in nucleotide excision repair-deficient lymphoblastoid cells 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Gopalakrishnan et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (<url>http://creativecommons.org/licenses/by/2.0</url>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background The Nucleotide Excision Repair (NER) pathway specialises in UV-induced DNA damage repair. Inherited defects in the NER can predispose individuals to Xeroderma Pigmentosum (XP). UV-induced DNA damage cannot account for the manifestation of XP in organ systems not directly exposed to sunlight. While the NER has recently been implicated in the repair of oxidative DNA lesions, it is not well characterised. Therefore we sought to investigate the role of NER factors Xeroderma Pigmentosum A (XPA), XPB and XPD in oxidative DNA damage-repair by subjecting lymphoblastoid cells from patients suffering from XP-A, XP-D and XP-B with Cockayne Syndrome to hydrogen peroxide ($ H_{2} %$ O_{2} $). Results Loss of functional XPB or XPD but not XPA led to enhanced sensitivity towards $ H_{2} %$ O_{2} $-induced cell death. XP-deficient lymphoblastoid cells exhibited increased susceptibility to $ H_{2} %$ O_{2} $-induced DNA damage with XPD showing the highest susceptibility and lowest repair capacity. Furthermore, XPB- and XPD-deficient lymphoblastoid cells displayed enhanced DNA damage at the telomeres. XPA- and XPB-deficient lymphoblastoid cells also showed differential regulation of XPD following $ H_{2} %$ O_{2} $ treatment. Conclusions Taken together, our data implicate a role for the NER in $ H_{2} %$ O_{2} $-induced oxidative stress management and further corroborates that oxidative stress is a significant contributing factor in XP symptoms. Resistance of XPA-deficient lymphoblastoid cells to $ H_{2} %$ O_{2} $-induced cell death while harbouring DNA damage poses a potential cancer risk factor for XPA patients. Our data implicate XPB and XPD in the protection against oxidative stress-induced DNA damage and telomere shortening, and thus premature senescence. Nucleotide Excision Repair (dpeaa)DE-He213 Base Excision Repair (dpeaa)DE-He213 Xeroderma Pigmentosum (dpeaa)DE-He213 Tail Moment (dpeaa)DE-He213 Cockayne Syndrome (dpeaa)DE-He213 Low, Grace Kah Mun aut Ting, Aloysius Poh Leong aut Srikanth, Prarthana aut Slijepcevic, Predrag aut Hande, M Prakash aut Enthalten in Genome integrity Cham, Switzerland : Springer International Publishing AG, 2010 1(2010), 1 vom: 22. Dez. (DE-627)627611745 (DE-600)2556795-0 2041-9414 nnns volume:1 year:2010 number:1 day:22 month:12 https://dx.doi.org/10.1186/2041-9414-1-16 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 1 2010 1 22 12 |
| allfieldsGer |
10.1186/2041-9414-1-16 doi (DE-627)SPR030900220 (SPR)2041-9414-1-16-e DE-627 ger DE-627 rakwb eng Gopalakrishnan, Kalpana verfasserin aut Hydrogen peroxide induced genomic instability in nucleotide excision repair-deficient lymphoblastoid cells 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Gopalakrishnan et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (<url>http://creativecommons.org/licenses/by/2.0</url>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background The Nucleotide Excision Repair (NER) pathway specialises in UV-induced DNA damage repair. Inherited defects in the NER can predispose individuals to Xeroderma Pigmentosum (XP). UV-induced DNA damage cannot account for the manifestation of XP in organ systems not directly exposed to sunlight. While the NER has recently been implicated in the repair of oxidative DNA lesions, it is not well characterised. Therefore we sought to investigate the role of NER factors Xeroderma Pigmentosum A (XPA), XPB and XPD in oxidative DNA damage-repair by subjecting lymphoblastoid cells from patients suffering from XP-A, XP-D and XP-B with Cockayne Syndrome to hydrogen peroxide ($ H_{2} %$ O_{2} $). Results Loss of functional XPB or XPD but not XPA led to enhanced sensitivity towards $ H_{2} %$ O_{2} $-induced cell death. XP-deficient lymphoblastoid cells exhibited increased susceptibility to $ H_{2} %$ O_{2} $-induced DNA damage with XPD showing the highest susceptibility and lowest repair capacity. Furthermore, XPB- and XPD-deficient lymphoblastoid cells displayed enhanced DNA damage at the telomeres. XPA- and XPB-deficient lymphoblastoid cells also showed differential regulation of XPD following $ H_{2} %$ O_{2} $ treatment. Conclusions Taken together, our data implicate a role for the NER in $ H_{2} %$ O_{2} $-induced oxidative stress management and further corroborates that oxidative stress is a significant contributing factor in XP symptoms. Resistance of XPA-deficient lymphoblastoid cells to $ H_{2} %$ O_{2} $-induced cell death while harbouring DNA damage poses a potential cancer risk factor for XPA patients. Our data implicate XPB and XPD in the protection against oxidative stress-induced DNA damage and telomere shortening, and thus premature senescence. Nucleotide Excision Repair (dpeaa)DE-He213 Base Excision Repair (dpeaa)DE-He213 Xeroderma Pigmentosum (dpeaa)DE-He213 Tail Moment (dpeaa)DE-He213 Cockayne Syndrome (dpeaa)DE-He213 Low, Grace Kah Mun aut Ting, Aloysius Poh Leong aut Srikanth, Prarthana aut Slijepcevic, Predrag aut Hande, M Prakash aut Enthalten in Genome integrity Cham, Switzerland : Springer International Publishing AG, 2010 1(2010), 1 vom: 22. Dez. (DE-627)627611745 (DE-600)2556795-0 2041-9414 nnns volume:1 year:2010 number:1 day:22 month:12 https://dx.doi.org/10.1186/2041-9414-1-16 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 1 2010 1 22 12 |
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10.1186/2041-9414-1-16 doi (DE-627)SPR030900220 (SPR)2041-9414-1-16-e DE-627 ger DE-627 rakwb eng Gopalakrishnan, Kalpana verfasserin aut Hydrogen peroxide induced genomic instability in nucleotide excision repair-deficient lymphoblastoid cells 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Gopalakrishnan et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (<url>http://creativecommons.org/licenses/by/2.0</url>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background The Nucleotide Excision Repair (NER) pathway specialises in UV-induced DNA damage repair. Inherited defects in the NER can predispose individuals to Xeroderma Pigmentosum (XP). UV-induced DNA damage cannot account for the manifestation of XP in organ systems not directly exposed to sunlight. While the NER has recently been implicated in the repair of oxidative DNA lesions, it is not well characterised. Therefore we sought to investigate the role of NER factors Xeroderma Pigmentosum A (XPA), XPB and XPD in oxidative DNA damage-repair by subjecting lymphoblastoid cells from patients suffering from XP-A, XP-D and XP-B with Cockayne Syndrome to hydrogen peroxide ($ H_{2} %$ O_{2} $). Results Loss of functional XPB or XPD but not XPA led to enhanced sensitivity towards $ H_{2} %$ O_{2} $-induced cell death. XP-deficient lymphoblastoid cells exhibited increased susceptibility to $ H_{2} %$ O_{2} $-induced DNA damage with XPD showing the highest susceptibility and lowest repair capacity. Furthermore, XPB- and XPD-deficient lymphoblastoid cells displayed enhanced DNA damage at the telomeres. XPA- and XPB-deficient lymphoblastoid cells also showed differential regulation of XPD following $ H_{2} %$ O_{2} $ treatment. Conclusions Taken together, our data implicate a role for the NER in $ H_{2} %$ O_{2} $-induced oxidative stress management and further corroborates that oxidative stress is a significant contributing factor in XP symptoms. Resistance of XPA-deficient lymphoblastoid cells to $ H_{2} %$ O_{2} $-induced cell death while harbouring DNA damage poses a potential cancer risk factor for XPA patients. Our data implicate XPB and XPD in the protection against oxidative stress-induced DNA damage and telomere shortening, and thus premature senescence. Nucleotide Excision Repair (dpeaa)DE-He213 Base Excision Repair (dpeaa)DE-He213 Xeroderma Pigmentosum (dpeaa)DE-He213 Tail Moment (dpeaa)DE-He213 Cockayne Syndrome (dpeaa)DE-He213 Low, Grace Kah Mun aut Ting, Aloysius Poh Leong aut Srikanth, Prarthana aut Slijepcevic, Predrag aut Hande, M Prakash aut Enthalten in Genome integrity Cham, Switzerland : Springer International Publishing AG, 2010 1(2010), 1 vom: 22. Dez. (DE-627)627611745 (DE-600)2556795-0 2041-9414 nnns volume:1 year:2010 number:1 day:22 month:12 https://dx.doi.org/10.1186/2041-9414-1-16 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 1 2010 1 22 12 |
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Hydrogen peroxide induced genomic instability in nucleotide excision repair-deficient lymphoblastoid cells |
| abstract |
Background The Nucleotide Excision Repair (NER) pathway specialises in UV-induced DNA damage repair. Inherited defects in the NER can predispose individuals to Xeroderma Pigmentosum (XP). UV-induced DNA damage cannot account for the manifestation of XP in organ systems not directly exposed to sunlight. While the NER has recently been implicated in the repair of oxidative DNA lesions, it is not well characterised. Therefore we sought to investigate the role of NER factors Xeroderma Pigmentosum A (XPA), XPB and XPD in oxidative DNA damage-repair by subjecting lymphoblastoid cells from patients suffering from XP-A, XP-D and XP-B with Cockayne Syndrome to hydrogen peroxide ($ H_{2} %$ O_{2} $). Results Loss of functional XPB or XPD but not XPA led to enhanced sensitivity towards $ H_{2} %$ O_{2} $-induced cell death. XP-deficient lymphoblastoid cells exhibited increased susceptibility to $ H_{2} %$ O_{2} $-induced DNA damage with XPD showing the highest susceptibility and lowest repair capacity. Furthermore, XPB- and XPD-deficient lymphoblastoid cells displayed enhanced DNA damage at the telomeres. XPA- and XPB-deficient lymphoblastoid cells also showed differential regulation of XPD following $ H_{2} %$ O_{2} $ treatment. Conclusions Taken together, our data implicate a role for the NER in $ H_{2} %$ O_{2} $-induced oxidative stress management and further corroborates that oxidative stress is a significant contributing factor in XP symptoms. Resistance of XPA-deficient lymphoblastoid cells to $ H_{2} %$ O_{2} $-induced cell death while harbouring DNA damage poses a potential cancer risk factor for XPA patients. Our data implicate XPB and XPD in the protection against oxidative stress-induced DNA damage and telomere shortening, and thus premature senescence. © Gopalakrishnan et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (<url>http://creativecommons.org/licenses/by/2.0</url>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
| abstractGer |
Background The Nucleotide Excision Repair (NER) pathway specialises in UV-induced DNA damage repair. Inherited defects in the NER can predispose individuals to Xeroderma Pigmentosum (XP). UV-induced DNA damage cannot account for the manifestation of XP in organ systems not directly exposed to sunlight. While the NER has recently been implicated in the repair of oxidative DNA lesions, it is not well characterised. Therefore we sought to investigate the role of NER factors Xeroderma Pigmentosum A (XPA), XPB and XPD in oxidative DNA damage-repair by subjecting lymphoblastoid cells from patients suffering from XP-A, XP-D and XP-B with Cockayne Syndrome to hydrogen peroxide ($ H_{2} %$ O_{2} $). Results Loss of functional XPB or XPD but not XPA led to enhanced sensitivity towards $ H_{2} %$ O_{2} $-induced cell death. XP-deficient lymphoblastoid cells exhibited increased susceptibility to $ H_{2} %$ O_{2} $-induced DNA damage with XPD showing the highest susceptibility and lowest repair capacity. Furthermore, XPB- and XPD-deficient lymphoblastoid cells displayed enhanced DNA damage at the telomeres. XPA- and XPB-deficient lymphoblastoid cells also showed differential regulation of XPD following $ H_{2} %$ O_{2} $ treatment. Conclusions Taken together, our data implicate a role for the NER in $ H_{2} %$ O_{2} $-induced oxidative stress management and further corroborates that oxidative stress is a significant contributing factor in XP symptoms. Resistance of XPA-deficient lymphoblastoid cells to $ H_{2} %$ O_{2} $-induced cell death while harbouring DNA damage poses a potential cancer risk factor for XPA patients. Our data implicate XPB and XPD in the protection against oxidative stress-induced DNA damage and telomere shortening, and thus premature senescence. © Gopalakrishnan et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (<url>http://creativecommons.org/licenses/by/2.0</url>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
| abstract_unstemmed |
Background The Nucleotide Excision Repair (NER) pathway specialises in UV-induced DNA damage repair. Inherited defects in the NER can predispose individuals to Xeroderma Pigmentosum (XP). UV-induced DNA damage cannot account for the manifestation of XP in organ systems not directly exposed to sunlight. While the NER has recently been implicated in the repair of oxidative DNA lesions, it is not well characterised. Therefore we sought to investigate the role of NER factors Xeroderma Pigmentosum A (XPA), XPB and XPD in oxidative DNA damage-repair by subjecting lymphoblastoid cells from patients suffering from XP-A, XP-D and XP-B with Cockayne Syndrome to hydrogen peroxide ($ H_{2} %$ O_{2} $). Results Loss of functional XPB or XPD but not XPA led to enhanced sensitivity towards $ H_{2} %$ O_{2} $-induced cell death. XP-deficient lymphoblastoid cells exhibited increased susceptibility to $ H_{2} %$ O_{2} $-induced DNA damage with XPD showing the highest susceptibility and lowest repair capacity. Furthermore, XPB- and XPD-deficient lymphoblastoid cells displayed enhanced DNA damage at the telomeres. XPA- and XPB-deficient lymphoblastoid cells also showed differential regulation of XPD following $ H_{2} %$ O_{2} $ treatment. Conclusions Taken together, our data implicate a role for the NER in $ H_{2} %$ O_{2} $-induced oxidative stress management and further corroborates that oxidative stress is a significant contributing factor in XP symptoms. Resistance of XPA-deficient lymphoblastoid cells to $ H_{2} %$ O_{2} $-induced cell death while harbouring DNA damage poses a potential cancer risk factor for XPA patients. Our data implicate XPB and XPD in the protection against oxidative stress-induced DNA damage and telomere shortening, and thus premature senescence. © Gopalakrishnan et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (<url>http://creativecommons.org/licenses/by/2.0</url>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
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Hydrogen peroxide induced genomic instability in nucleotide excision repair-deficient lymphoblastoid cells |
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Low, Grace Kah Mun Ting, Aloysius Poh Leong Srikanth, Prarthana Slijepcevic, Predrag Hande, M Prakash |
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