William J. Bodell

University of California, San Francisco

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Krisztina Pongracz

Geron (United States)

György Lévay

Semmelweis University

Deena Nath Pathak

University of California, San Francisco

Toshimitsu Aida

Hokkaido Orthopedic Surgery Memorial Hospital

James E. Cleaver

University of California, San Francisco

Mark L. Rosenblum

Henry Ford Health System

Jytte Rasmussen

University of California, Berkeley

Mitchel S. Berger

University of California, San Francisco

Nilesh W. Gaikwad

University of California, Davis

Kouichi Tokuda

Wakaba Hospital

Cooperative Institutions

University of California, San Francisco

Neurological Surgery

University of California, Berkeley

Harvard University

Lawrence Berkeley National Laboratory

National Cancer Institute

University of North Carolina at Chapel Hill

Massachusetts General Hospital

University of Nebraska Medical Center

University of Washington

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³²P-Post-labeling detection of DNA adducts in mononuclear cells of workers occupationally exposed to styrene

Carcinogenesis (1994)

Éva Horváth Krisztina Pongracz Stephen M. Rappaport William J. Bodell

Journal Article 32P-Post-labeling detection of DNA adducts in mononuclear cells of workers occupationally exposed to styrene Get access Eva Horvath, Eva Horvath 1Brain Tumor Research Center of the Department of Neurological Surgery, University of CaliforniaSan Francisco, CA 94143–0806 USA Search for other works by this author on: Oxford Academic PubMed Google Scholar Krisztina Pongracz, Krisztina Pongracz 1Brain Tumor Research Center of the Department of Neurological Surgery, University of CaliforniaSan Francisco, CA 94143–0806 USA Search for other works by this author on: Oxford Academic PubMed Google Scholar Stephen Rappaport, Stephen Rappaport 2Department of Environmental Science and Engineering, School of Public Health, University of North CarolinaChapel Hill, NC, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar William J. Bodell William J. Bodell 3 1Brain Tumor Research Center of the Department of Neurological Surgery, University of CaliforniaSan Francisco, CA 94143–0806 USA 3To whom correspondence should be addressed Search for other works by this author on: Oxford Academic PubMed Google Scholar Carcinogenesis, Volume 15, Issue 7, July 1994, Pages 1309–1315, https://doi.org/10.1093/carcin/15.7.1309 Published: 01 July 1994 Article history Received: 22 September 1993 Revision received: 07 April 1994 Accepted: 14 April 1994 Published: 01 July 1994

Rappaport

New england

10.1093/carcin/15.7.1309

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Citations (35)

Effect of caffeine on cytotoxicity and sister chromatid exchange induction in sensitive and resistant rat brain tumor cells treated with 1,3-bis(2-chloroethyl)-1-nitrosourea.

PubMed (1987)

Toshimitsu Aida William J. Bodell

Treatment of 9L and 9L-2 cells, which are, respectively, sensitive and resistant to 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), with various concentrations of BCNU followed by treatment with 1 mM caffeine potentiated BCNU cytotoxicity by 10-fold with dose modification factors of 1.5 to 1.7. The synergistic effect of caffeine on cellular toxicity diminished when caffeine was added 6 to 24 h after treatment of BCNU. The number of sister chromatid exchanges (SCEs) induced by treatment with BCNU in both cell lines showed a good correlation with cytotoxicity; the number of SCEs induced in 9L cells is 6-fold higher than the number induced in 9L-2 cells. Caffeine potentiated BCNU induction of SCEs in both 9L or 9L-2 cells by the same amount. Caffeine potentiation of BCNU-induced SCEs was also time dependent and was eliminated by a delay of 6 h between BCNU treatment and addition of caffeine. Caffeine had no effect on the formation and removal of DNA cross-links in either 9L or 9L-2 cells after BCNU treatment as determined with the alkaline elution assay. Eighteen to 24 h after BCNU treatment there was an accumulation of 9L cells in late-S-G2-M phase of the cell cycle which diminished with time. Caffeine treatment potentiated the BCNU-induced accumulation of cells in late-S-G2-M phase of the cell cycle. Our results suggest that caffeine potentiates BCNU cytotoxicity and induction of SCEs by a mechanism that is independent of repair of alkylation products, but that may depend on alterations of cellular replication in BCNU-treated cells.

Carmustine

Sister chromatid exchange

Nitrosourea

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Citations (15)

Auger electron contribution to bromodeoxyuridine cellular radiosensitization

International Journal of Radiation Oncology*Biology*Physics (1989)

David A. Larson William J. Bodell C. Clifton Ling Theodore L. Phillips M.C. Schell

Auger effect

Photoelectric effect

Absorption edge

Bromodeoxyuridine

Thymidine

10.1016/0360-3016(89)90025-4

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Citations (34)

The influence of chromatin structure on the distribution of DNA repair synthesis studied by nuclease digestion

Nucleic Acids Research (1979)

William J. Bodell Mihir R. Banerjee

Journal Article The influence of chromatin structure on the distribution of DNA repair synthesis studied by nuclease digestion Get access William J. Bodell, William J. Bodell Tumor Biology Laboratory, School of Life Sciences, University of NebraskaLincoln, NE 68588, USA 1 Present Address: Department of Molecular Biology and Virus Laboratory, University of California, Berkeley, California 94720. Search for other works by this author on: Oxford Academic PubMed Google Scholar Mihir R. Banerjee Mihir R. Banerjee Tumor Biology Laboratory, School of Life Sciences, University of NebraskaLincoln, NE 68588, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar Nucleic Acids Research, Volume 6, Issue 1, 1 January 1979, Pages 359–370, https://doi.org/10.1093/nar/6.1.359 Published: 01 January 1979 Article history Received: 08 September 1978 Published: 01 January 1979

Nuclease

10.1093/nar/6.1.359

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Citations (35)

An investigation of multiple biomarkers among workers exposed to styrene and styrene-7,8-oxide.

PubMed (1996)

Stephen M. Rappaport Karen Yeowell-O’Connell William J. Bodell Janice W. Yager Elaine Symanski

Investigations of cancer and cytogenetic damage among reinforced-plastics workers have produced contradictory results. In all studies, the focus has been on styrene rather than the carcinogen, styrene-7,8-oxide (SO), traces of which are generated during the manufacturing process. Because styrene is present at very high levels and is metabolized almost exclusively through SO, coexposures to SO have been discounted. This study investigated the relative contributions of airborne styrene and SO and of smoking toward several SO-specific biomarkers (DNA and albumin adducts) and sister chromatid exchanges in the blood of 48 reinforced-plastics workers. Among individual subjects, albumin and DNA adducts as well as sister chromatid exchanges were significantly correlated with styrene exposure. However, among the 20 subjects with measurements to both styrene and SO, albumin adducts were significantly correlated with exposure to SO but not to styrene. Finally, among the 10 job groups, surprisingly strong correlations (0.709 < or = r < or = 0.966) were found between all SO biomarkers and exposure to SO but not to styrene. Calculations suggest that SO was about 2000 times more effective than styrene in producing SO biomarkers. After accounting for the disparate exposures to the two chemicals, a typical worker received 71% of the systemic dose of SO via inhalation; nonetheless, 5 of the 20 subjects received the majority of the SO dose from styrene. Cigarette smoking increased levels of SO-albumin and SO-DNA adducts, suggesting that SO was a constituent of tobacco smoke. We conclude that inhalation of SO should be considered in any interventions to reduce health risks.

Sister chromatid exchange

Inhalation exposure

Styrene oxide

Clastogen

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Citations (49)

Potentiation of DNA adduct formation in HL-60 cells by combinations of benzene metabolites.

Proceedings of the National Academy of Sciences (1992)

György Lévay William J. Bodell

Using P1 nuclease enhanced 32P postlabeling, we investigated DNA adduct formation in HL-60 promyelocytic leukemia cells treated with the benzene metabolites hydroquinone, catechol, and 1,2,4-benzenetriol. Comparison of the slopes of the dose-response curves showed that hydroquinone was 7-9 times more effective than 1,2,4,-benzenetriol and catechol at inducing DNA adducts. Comparison of hydroquinone with catechol showed a good correlation between adduct formation and cytotoxicity. Similar comparisons of hydroquinone and 1,2,4,-benzenetriol suggest that cellular processes in addition to DNA adduct formation contributed to cytotoxicity. In cells treated with the combination of hydroquinone and either catechol or 1,2,4,-benzenetriol, DNA adduct formation was 3-6 times greater than the sum of adduct formation produced by single-agent treatments. Treatment with hydroquinone and 1,2,4,-benzenetriol produced DNA adducts not detected after treatment with either metabolite alone. The synergistic interaction of benzene metabolites in the production of DNA adducts may play an important role in the genotoxic effects of benzene in vivo.

Hydroquinone

Catechol

10.1073/pnas.89.15.7105

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Citations (59)

Investigation of the DNA adducts formed in B6C3F1 mice treated with benzene: implications for molecular dosimetry.

Environmental Health Perspectives (1996)

William J. Bodell Deena Nath Pathak György Lévay Q Ye Krisztina Pongracz

We have investigated the formation of DNA adducts in the bone marrow and white blood cells of male B6C3F1 mice treated with benzene using P1-enhanced 32P-postlabeling. No adducts were detected in the bone marrow of controls or mice treated with various doses of benzene once a day. After twice-daily treatment for 1 to 7 days with benzene, 440 mg/kg, one major (no. 1) and up to two minor DNA adducts were detected in both the bone marrow and white blood cells. The relative adduct levels in these cells ranged from 0.06 to 1.46 x 10(-7). a significant correlation (r2 = 0.95) between levels of adducts in bone marrow and white blood cells was observed. After a 7-day treatment with benzene, 440 mg/kg twice a day, the number of cells per femur decreased from 1.6 x 10(7) to 0.85 x 10(7), indicating myelotoxicity. In contrast, administration of benzene once a day produced only a small decrease in bone marrow cellularity. The observed induction of toxicity in bone marrow was paralleled by formation of DNA adducts. In vitro treatment of bone marrow with hydroquinone (HQ) for 24 hr produced the same DNA adducts as found after treatment of mice with benzene, suggesting that HQ is the principal metabolite of benzene leading to DNA adduct formation in vivo. Using P-postlabeling the principal DNA adduct formed in vivo was compared with N2-(4-hydroxyphenyl)-2'-deoxyguanosine-3'-phosphate. The results of this comparison demonstrated that the DNA adduct formed in vivo co-chromatographs with N2-(4-hydroxyphenyl)-2'-deoxyguanosine-3'-phosphate. These studies indicate that metabolic activation of benzene leads to the formation of DNA adducts in bone marrow and white blood cells and suggest that measurement of DNA adducts in white blood cells may be an indicator of biological effect following benzene exposure.

Hydroquinone

DNA adduct

Deoxyguanosine

10.1289/ehp.961041189

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Citations (43)

Effect of Cations on the Formation of DNA Alkylation Products in DNA Reacted with 1-(2-Chloroethyl)-1-nitrosourea

Chemical Research in Toxicology (1999)

William J. Bodell

The purpose of this study was to examine the influence of cations on the formation of the individual DNA alkylation products derived from 1-(2-chloroethyl)-1-nitrosourea (CNU). Reaction of calf-thymus DNA with [3H]CNU in 10 mM triethanolamine buffer produced 13 DNA adducts. Seven of these adducts were identified as N7-(2-hydroxyethyl)guanine, N7-(2-chloroethyl)guanine, 1,2-(diguan-7-yl)ethane, N1-(2-hydroxyethyl)-2-deoxyguanosine, 1-(N1-2-deoxyguanosinyl)-2-(N3-2-deoxycytidyl)ethane, O6-(2-hydroxyethyl)-2-deoxyguanosine, and phosphotriesters. The ratios of the individual products indicated that the chloroethyl and hydroxyethyl adducts are derived from different alkylating intermediates. The influence of cations on the formation of these DNA alkylation products was investigated by the addition of either NaCl, MgCl2, or spermine. The results demonstrated that (1) the levels of DNA alkylation were inversely proportional to ionic strength, (2) the extent of inhibition was dependent on the alkylation product, and (3) the order of relative effectiveness of inhibition of DNA alkylation by these cations was as follows: spermine > Mg > Na. These results support a model whereby reactions which proceed via an SN2 mechanism are more sensitive to the effects of ionic strength than reactions which proceed via an SN1 mechanism. In 9L cells treated with CNU, the same alkylation products were formed as in purified DNA; however, the product distribution was different. We interpret this to indicate that within cells, cations modify the reaction of intermediates derived from CNU with DNA.

Deoxyguanosine

10.1021/tx980200c

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Citations (21)

Distribution of DNA repair in chromatin

Mutation Research/Environmental Mutagenesis and Related Subjects (1978)

William J. Bodell

Micrococcal nuclease

Nuclease

10.1016/0165-1161(78)90457-0

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Citations (0)

SHORT COMMUNICATION: Detection of DNA adducts in the white blood cells of B6C3F1 mice treated with benzene

Carcinogenesis (1996)

György Lévay Deena Nath Pathak William J. Bodell

We have employed the P1-enhanced 32P-postlabeling procedure to detect the formation DNA of adducts in the white blood cells (WBC) of B6C3F1 mice treated by i.p. injection with benzene. Treatment twice a day with 440 mg/kg benzene for 1–7 days resulted in the formation of one major (adduct 1) and one minor (adduct 2) DNA adduct in the WBCs of mice. The same DNA adduct pattern was also found in the bone marrow (BM) of benzene treated mice. The relative adduct levels were dependent upon both benzene dose from 100–440 mg/kg and treatment time from 1 to 7 days. The relative adduct levels ranged between 0.11 and 1.33 adducts in 107 nucleotides for WBCs and 0.16–1.21 adducts in 107 nucleotides for BM. Following treatment with benzene, the levels of DNA adducts formed in WBCs were significantly correlated with the levels of DNA adducts formed in BM (r2 = 0.97, P <0.001). Our results suggest that measurement of DNA adducts in WBCs may be an indicator of DNA adduct formation in BM following BZ exposure.

White (mutation)

10.1093/carcin/17.1.151

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Citations (18)