Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1992-7-21
pubmed:abstractText
If excision repair-proficient human cells are allowed time for repair before onset of S phase, the premutagenic lesions formed by (+/-)-7 beta,8 alpha-dihydroxy-9 alpha,10 alpha-epoxy- 7,8,9,10-tetrahydrobenzo[a]pyrene (benzo[a]pyrene diol epoxide, BPDE) are lost from the transcribed strand of the hypoxanthine (guanine) phosphoribosyltransferase (HPRT) gene faster than from the nontranscribed strand. No change in strand distribution is seen with repair-deficient cells. These results suggest strand-specific repair of BPDE-induced DNA damage in human cells. To test this, we measured the initial number of BPDE adducts formed in each strand of the actively transcribed HPRT gene and the rate of repair, using UvrABC excinuclease in conjunction with Southern hybridization and strand-specific probes. We also measured the rate of loss of BPDE adducts from the inactive 754 locus. The frequencies of adducts formed by exposure to BPDE (1.0 or 1.2 microM) in either strand of a 20-kilobase fragment that lies entirely within the transcription unit of the HPRT gene were similar; the frequency in the 14-kilobase 754 fragment was approximately 20% lower. The rates of repair in the two strands of the HPRT fragment differed significantly. Within 7 hr after treatment with 1.2 microM BPDE, 53% of the adducts had been removed from the transcribed strand, but only 26% from the nontranscribed strand; after 20 hr, these values were 87% and 58%, respectively. In contrast, only approximately 14% of the BPDE adducts were lost from the 754 locus in 20 hr, a value even lower than the rate of loss from the overall genome (i.e., 38%). These results demonstrate strand-specific and preferential repair of BPDE adducts in human cells. They suggest that the heterogeneous repair of BPDE adducts in the human genome cannot be accounted for merely by the greatly increased rate of the repair specific to the transcribed strand of the active genes, and they point to a role for the chromatin structure.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-1551881, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-1649389, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-1674998, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-1688519, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-1896474, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-1899045, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-1902394, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-1906131, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-2056910, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-2062855, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-2122466, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-2308842, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-2342504, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-2554145, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-2760069, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-2827103, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-2835822, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-2877935, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-3023360, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-3041622, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-3062380, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-3080255, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-3664636, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-3838150, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-3922635, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-3932847, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-427125, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-445470, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-6091052, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-6280150, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-6312838, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-6397773, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-6704400, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608950-6791861
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0027-8424
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
89
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5413-7
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Preferential repair and strand-specific repair of benzo[a]pyrene diol epoxide adducts in the HPRT gene of diploid human fibroblasts.
pubmed:affiliation
Department of Microbiology, Michigan State University, East Lansing 48824-1316.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.