An analysis of the mutagenicity of 1,2-dibromoethane to Escherichia coli: Influence of DNA repair activities and metabolic pathways

Patricia L. Foster; Wells G. Wilkinson; Judith K. Miller; Amy D. Sullivan; Wane M. Barnes

doi:10.1016/0167-8817(88)90019-3

An analysis of the mutagenicity of 1,2-dibromoethane to Escherichia coli: Influence of DNA repair activities and metabolic pathways

Patricia L. Foster, Wells G. Wilkinson, Judith K. Miller, Amy D. Sullivan, Wane M. Barnes

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Abstract

The mutagenicity of 1,2-dibromoethane (EDB) to Escherichia coli was reduced by the UV light-induced excision repair system but unaffected by the loss of a major apurinic/apyrimidinic site repair function. At high doses, 70-90% of the EDB-induced mutations were independent of SOS-mutagenic processing and approximately 50% were independent of glutathione conjugation. The SOS-independent mutations induced by EDB were unaffected by the enzymes that repair alkylation-induced DNA lesions. EDB-induced base substitutions were dominated by GC to AT and AT to GC transitions. These results suggest that EDB-induced premutagenic lesions have some, but not all, of the characteristics of simple alkyl lesions.

Original language	English
Pages (from-to)	171-181
Number of pages	11
Journal	Mutation Research DNA Repair Reports
Volume	194
Issue number	3
DOIs	https://doi.org/10.1016/0167-8817(88)90019-3
State	Published - Nov 1988

Keywords

DNA repair
Dibromoethane
EDB
Escherichia coli
Miscoding lesions

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10.1016/0167-8817(88)90019-3

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@article{c84518fe96924e27928f5c1131a2f269,

title = "An analysis of the mutagenicity of 1,2-dibromoethane to Escherichia coli: Influence of DNA repair activities and metabolic pathways",

abstract = "The mutagenicity of 1,2-dibromoethane (EDB) to Escherichia coli was reduced by the UV light-induced excision repair system but unaffected by the loss of a major apurinic/apyrimidinic site repair function. At high doses, 70-90% of the EDB-induced mutations were independent of SOS-mutagenic processing and approximately 50% were independent of glutathione conjugation. The SOS-independent mutations induced by EDB were unaffected by the enzymes that repair alkylation-induced DNA lesions. EDB-induced base substitutions were dominated by GC to AT and AT to GC transitions. These results suggest that EDB-induced premutagenic lesions have some, but not all, of the characteristics of simple alkyl lesions.",

keywords = "DNA repair, Dibromoethane, EDB, Escherichia coli, Miscoding lesions",

author = "Foster, {Patricia L.} and Wilkinson, {Wells G.} and Miller, {Judith K.} and Sullivan, {Amy D.} and Barnes, {Wane M.}",

note = "Funding Information: This work was supported by National Institutes of Health Grants CA37880 to P.L.F. and GM24956 to W.M.B. and American Cancer Society (Massachusetts Division) Institutional Grant for Faculty Research IN-97H to P.L.F.",

year = "1988",

month = nov,

doi = "10.1016/0167-8817(88)90019-3",

language = "English",

volume = "194",

pages = "171--181",

journal = "Mutation Research DNA Repair Reports",

issn = "0167-8817",

number = "3",

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TY - JOUR

T1 - An analysis of the mutagenicity of 1,2-dibromoethane to Escherichia coli

T2 - Influence of DNA repair activities and metabolic pathways

AU - Foster, Patricia L.

AU - Wilkinson, Wells G.

AU - Miller, Judith K.

AU - Sullivan, Amy D.

AU - Barnes, Wane M.

N1 - Funding Information: This work was supported by National Institutes of Health Grants CA37880 to P.L.F. and GM24956 to W.M.B. and American Cancer Society (Massachusetts Division) Institutional Grant for Faculty Research IN-97H to P.L.F.

PY - 1988/11

Y1 - 1988/11

N2 - The mutagenicity of 1,2-dibromoethane (EDB) to Escherichia coli was reduced by the UV light-induced excision repair system but unaffected by the loss of a major apurinic/apyrimidinic site repair function. At high doses, 70-90% of the EDB-induced mutations were independent of SOS-mutagenic processing and approximately 50% were independent of glutathione conjugation. The SOS-independent mutations induced by EDB were unaffected by the enzymes that repair alkylation-induced DNA lesions. EDB-induced base substitutions were dominated by GC to AT and AT to GC transitions. These results suggest that EDB-induced premutagenic lesions have some, but not all, of the characteristics of simple alkyl lesions.

AB - The mutagenicity of 1,2-dibromoethane (EDB) to Escherichia coli was reduced by the UV light-induced excision repair system but unaffected by the loss of a major apurinic/apyrimidinic site repair function. At high doses, 70-90% of the EDB-induced mutations were independent of SOS-mutagenic processing and approximately 50% were independent of glutathione conjugation. The SOS-independent mutations induced by EDB were unaffected by the enzymes that repair alkylation-induced DNA lesions. EDB-induced base substitutions were dominated by GC to AT and AT to GC transitions. These results suggest that EDB-induced premutagenic lesions have some, but not all, of the characteristics of simple alkyl lesions.

KW - DNA repair

KW - Dibromoethane

KW - EDB

KW - Escherichia coli

KW - Miscoding lesions

UR - http://www.scopus.com/inward/record.url?scp=0023797379&partnerID=8YFLogxK

U2 - 10.1016/0167-8817(88)90019-3

DO - 10.1016/0167-8817(88)90019-3

M3 - Article

C2 - 3054522

AN - SCOPUS:0023797379

SN - 0167-8817

VL - 194

SP - 171

EP - 181

JO - Mutation Research DNA Repair Reports

JF - Mutation Research DNA Repair Reports

IS - 3

ER -

An analysis of the mutagenicity of 1,2-dibromoethane to Escherichia coli: Influence of DNA repair activities and metabolic pathways

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Keywords

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