Double Base Lesions in DNA X-Irradiated in the Presence or Absence of Oxygen

Abstract Box, H. C., Patrzyc, H. B., Dawidzik, J. B., Wallace, J. C., Freund, H. G., Iijima, H. and Budzinski, E. E. Double Base Lesions in DNA X-Irradiated in the Presence or Absence of Oxygen. Previously, double lesions in which two adjacent bases are modified were identified in DNA oligomers exposed in solution to ionizing radiation. However, the formation of such lesions in polymer DNA had not been demonstrated. Using reference oligomer containing a specific double lesion and employing liquid chromatography-mass spectrometry (LC-MS), it was possible to show directly that double lesions are formed in irradiated calf thymus DNA. The double lesion in which a pyrimidine base is degraded to a formamido remnant and an adjacent guanine base is oxidized to 8-oxoguanine was detected in DNA X-irradiated in oxygenated aqueous solution. The double lesion in which the methyl carbon atom of a thymine base is covalently linked to carbon at the 8-position of an adjacent guanine base was detected in DNA irradiated in a deoxygenated environment.

[1]  J. Wallace,et al.  Double-base lesions are produced in DNA by free radicals. , 2000, Archives of biochemistry and biophysics.

[2]  J. Wallace,et al.  Tandem lesions and other products in X-irradiated DNA oligomers. , 1998, Radiation research.

[3]  H. Box,et al.  Selective hydrolysis of damaged DNA by nuclease P1. , 1997, Biochimica et biophysica acta.

[4]  J. Wallace,et al.  Radiation-induced formation of a crosslink between base moieties of deoxyguanosine and thymidine in deoxygenated solutions of d(CpGpTpA). , 1996, Radiation research.

[5]  R. S. Sohal,et al.  Simultaneous Overexpression of Copper- and Zinc-containing Superoxide Dismutase and Catalase Retards Age-related Oxidative Damage and Increases Metabolic Potential in Drosophila melanogaster(*) , 1995, The Journal of Biological Chemistry.

[6]  W C Willett,et al.  The causes and prevention of cancer. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[7]  J. Wallace,et al.  The radiation chemistry of d(CpGpTpA) in the presence of oxygen. , 1995, Radiation research.

[8]  C. Sonntag,et al.  Topics in free radical-mediated DNA damage: purines and damage amplification-superoxic reactions-bleomycin, the incomplete radiomimetic , 1994 .

[9]  E. E. Budzinski,et al.  Free radical-induced tandem base damage in DNA oligomers. , 1997, Free radical biology & medicine.

[10]  J. Wallace,et al.  Isolation and characterization of the products of anoxic irradiation of d(CpGpTpA). , 1997, International journal of radiation biology.

[11]  J. Knight Reactive oxygen species and the neurodegenerative disorders. , 1997, Annals of clinical and laboratory science.

[12]  J. Wallace,et al.  Free radical-induced double base lesions. , 1995, Radiation research.

[13]  J. Wallace,et al.  Radiation chemistry of d(ApCpGpT). , 1995, International journal of radiation biology.

[14]  M S Evans,et al.  Vicinal lesions in X-irradiated DNA? , 1993, International journal of radiation biology.