Correlation of DNA adducts in blood mononuclear cells with tobacco carcinogen-induced damage in human lung. 1995

J K Wiencke, and K T Kelsey, and A Varkonyi, and K Semey, and J C Wain, and E Mark, and D C Christiani
Department of Epidemiology and Biostatistics, School of Medicine, University of California, San Francisco 94143-0560, USA.

The formation of carcinogen-DNA adducts within the respiratory epithelium is thought to be a critical factor in the induction of lung cancer from tobacco smoke. A reliable surrogate measure of carcinogen damage to the lung would be of great value in molecular epidemiological studies of cancer risk. The validity of measurements of DNA adducts formed from hydrophobic aromatic hydrocarbons in peripheral blood mononuclear cells (MNCs) was investigated by comparing the levels of aromatic DNA adducts detected in lung tissue from 31 lung cancer patients with those detected in MNCs from the same individuals using the 32P-postlabeling assay. The associations of smoking history and intake of dietary antioxidants with adduct levels also were assessed. Tissue-specific, as well as common DNA adducts were detected in lung and blood; total MNC adduct levels were highly correlated with total lung adducts. After smoking cessation, adduct levels appeared to decay in both tissues at similar rates. Multivariate analyses (Poisson regression modeling) indicated that dietary antioxidant intake (carotenoids, vitamin A, and retinol) modified the levels of aromatic DNA adducts in both the lungs and blood. Of all models tested, the optimal one for predicting lung adduct levels included the measure of blood MNC adduct levels only. Therefore, blood MNCs are a valid surrogate tissue for estimating the burden of DNA adducts in respiratory tissue in molecular epidemiological studies.

UI MeSH Term Description Entries
D007963 Leukocytes, Mononuclear Mature LYMPHOCYTES and MONOCYTES transported by the blood to the body's extravascular space. They are morphologically distinguishable from mature granulocytic leukocytes by their large, non-lobed nuclei and lack of coarse, heavily stained cytoplasmic granules. Mononuclear Leukocyte,Mononuclear Leukocytes,PBMC Peripheral Blood Mononuclear Cells,Peripheral Blood Human Mononuclear Cells,Peripheral Blood Mononuclear Cell,Peripheral Blood Mononuclear Cells,Leukocyte, Mononuclear
D008168 Lung Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood. Lungs
D008175 Lung Neoplasms Tumors or cancer of the LUNG. Cancer of Lung,Lung Cancer,Pulmonary Cancer,Pulmonary Neoplasms,Cancer of the Lung,Neoplasms, Lung,Neoplasms, Pulmonary,Cancer, Lung,Cancer, Pulmonary,Cancers, Lung,Cancers, Pulmonary,Lung Cancers,Lung Neoplasm,Neoplasm, Lung,Neoplasm, Pulmonary,Pulmonary Cancers,Pulmonary Neoplasm
D008297 Male Males
D008875 Middle Aged An adult aged 45 - 64 years. Middle Age
D002273 Carcinogens Substances that increase the risk of NEOPLASMS in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included. Carcinogen,Oncogen,Oncogens,Tumor Initiator,Tumor Initiators,Tumor Promoter,Tumor Promoters,Initiator, Tumor,Initiators, Tumor,Promoter, Tumor,Promoters, Tumor
D004247 DNA A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine). DNA, Double-Stranded,Deoxyribonucleic Acid,ds-DNA,DNA, Double Stranded,Double-Stranded DNA,ds DNA
D004249 DNA Damage Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION. These deviations may be caused by physical or chemical agents and occur by natural or unnatural, introduced circumstances. They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR). If the damage is extensive, it can induce APOPTOSIS. DNA Injury,DNA Lesion,DNA Lesions,Genotoxic Stress,Stress, Genotoxic,Injury, DNA,DNA Injuries
D005260 Female Females
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man

Related Publications

J K Wiencke, and K T Kelsey, and A Varkonyi, and K Semey, and J C Wain, and E Mark, and D C Christiani
December 2010, Carcinogenesis,
J K Wiencke, and K T Kelsey, and A Varkonyi, and K Semey, and J C Wain, and E Mark, and D C Christiani
November 2021, Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association,
J K Wiencke, and K T Kelsey, and A Varkonyi, and K Semey, and J C Wain, and E Mark, and D C Christiani
January 2002, Environmental and molecular mutagenesis,
J K Wiencke, and K T Kelsey, and A Varkonyi, and K Semey, and J C Wain, and E Mark, and D C Christiani
November 2000, Journal of the National Cancer Institute,
J K Wiencke, and K T Kelsey, and A Varkonyi, and K Semey, and J C Wain, and E Mark, and D C Christiani
January 2002, FASEB journal : official publication of the Federation of American Societies for Experimental Biology,
J K Wiencke, and K T Kelsey, and A Varkonyi, and K Semey, and J C Wain, and E Mark, and D C Christiani
November 1992, Nature,
J K Wiencke, and K T Kelsey, and A Varkonyi, and K Semey, and J C Wain, and E Mark, and D C Christiani
June 2005, Environmental research,
J K Wiencke, and K T Kelsey, and A Varkonyi, and K Semey, and J C Wain, and E Mark, and D C Christiani
January 2008, Mutagenesis,
J K Wiencke, and K T Kelsey, and A Varkonyi, and K Semey, and J C Wain, and E Mark, and D C Christiani
September 2008, Bulletin of experimental biology and medicine,
J K Wiencke, and K T Kelsey, and A Varkonyi, and K Semey, and J C Wain, and E Mark, and D C Christiani
January 1987, Progress in experimental tumor research,
Copied contents to your clipboard!