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Lead acetate mutagenicity and mutational spectrum in the hypoxanthine guanine phosphoribosyltransferase gene of Chinese hamster ovary K1 cells

Yang, Jia-Ling ; Yeh, Shie-Chie ; Chang, Chun-Yao

Molecular carcinogenesis, 1996-12, Vol.17 (4), p.181-191 [Peer Reviewed Journal]

New York: Wiley Subscription Services, Inc., A Wiley Company

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Title:
Lead acetate mutagenicity and mutational spectrum in the hypoxanthine guanine phosphoribosyltransferase gene of Chinese hamster ovary K1 cells
Author: Yang, Jia-Ling ; Yeh, Shie-Chie ; Chang, Chun-Yao
Subjects: Animals ; Base Sequence ; base substitutions ; CHO Cells - drug effects ; CHO Cells - enzymology ; CHO Cells - physiology ; Cricetinae ; deletions ; DNA Mutational Analysis ; DNA, Complementary - drug effects ; DNA, Complementary - genetics ; Drug Resistance ; Gene Deletion ; Hypoxanthine Phosphoribosyltransferase - genetics ; Lethal Dose 50 ; Molecular Sequence Data ; Mutagenesis ; Mutagens - toxicity ; Organometallic Compounds - toxicity ; Polymerase Chain Reaction ; Reverse transcriptase-polymerase chain reaction ; Sensitivity and Specificity ; sequencing ; Thioguanine - pharmacology ; Transcription, Genetic
Is Part Of: Molecular carcinogenesis, 1996-12, Vol.17 (4), p.181-191
Notes: istex:613894263441261DF19A9CFB21A2FB8BAD804206
ark:/67375/WNG-9228HQL2-N
ArticleID:MC2940170402
Description: The molecular nature of lead‐induced mutations was examined in this study to more thoroughly understand lead mutagenesis. Chinese hamster ovary K1 cells were exposed to 0.5–3 mM lead acetate for 24 h. The median lethal dose (LD,) value was 1.5 mM, and the hypoxanthine guanine phosphoribosyltransferase (HPRT) mutant frequency increased linearly as lead concentrations were raised from 0.5 to 1.5 mM. We also amplified the HPRTcDNAs of 56 independent lead‐induced mutants by reverse transcriptase‐polymerase chain reaction (PCR). Forty‐two mutant cDNAs were successfully amplified: 36 mutants had transcripts of normal or slightly smaller than normal size, and six mutants had large deletions. The other 14 mutants whose HPRTcDNA could not be amplified were subjected to genomic‐DNA PCR analysis. All of those mutants had one or more exons missing from their genomic HPRT DNA. DNA sequencing of mutant cDNAs showed that 22 had single‐base substitutions, four had small alterations, 10 had single‐exon deletions, and six were missing two or three exons. Furthermore, DNA sequencing of the HPRT intron‐exon boundaries in eight splice mutants revealed that all of them had single‐base substitutions in their genomic DNA. G.C base substitutions occurred 3.3‐fold more frequently than A.T base substitutions. Similar frequencies were observed for G.C → A.T, G.C → T.A, and GC → C.G mutations. These results suggest that GC base pairs may be the primary target sites for lead mutagenesis. © 1996 Wiley‐Liss, Inc.
Publisher: New York: Wiley Subscription Services, Inc., A Wiley Company
Language: English

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Lead acetate mutagenicity and mutational spectrum in the hypoxanthine guanine phosphoribosyltransferase gene of Chinese hamster ovary K1 cells

Yang, Jia-Ling ; Yeh, Shie-Chie ; Chang, Chun-Yao

New York: Wiley Subscription Services, Inc., A Wiley Company

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