Determination of Tobacco Specific Hemoglobin Adducts in Smoking Mothers and New Born Babies by Mass Spectrometry

Myers, Steven R.; Ali, Yeakub

doi:10.1177/117727190700200027

Cited by 11 publications

(4 citation statements)

References 68 publications

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“…Comparisons of paired maternal blood and cord blood levels of hemoglobin adducts derived from acrylamide, glycidamide and ethylene oxide indicate that the placenta gives little protection to the fetus from exposure to these compounds in utero 45. Nonsmoking mothers exposed to ETS during pregnancy had detectable levels of HPB‐releasing hemoglobin adducts, as did the fetal cord blood samples analyzed 198…”

Section: Exposure To Etsmentioning

confidence: 98%

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DNA and protein adducts in human tissues resulting from exposure to tobacco smoke

Phillips

Venitt

2012

Intl Journal of Cancer

124

122

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Tobacco smoke contains a variety of genotoxic carcinogens that form adducts with DNA and protein in the tissues of smokers. Not only are these biochemical events relevant to the carcinogenic process, but the detection of adducts provides a means of monitoring exposure to tobacco smoke. Characterization of smoking‐related adducts has shed light on the mechanisms of smoking‐related diseases and many different types of smoking‐derived DNA and protein adducts have been identified. Such approaches also reveal the potential harm of environmental tobacco smoke (ETS) to nonsmokers, infants and children. Because the majority of tobacco‐smoke carcinogens are not exclusive to this source of exposure, studies comparing smokers and nonsmokers may be confounded by other environmental sources. Nevertheless, certain DNA and protein adducts have been validated as biomarkers of exposure to tobacco smoke, with continuing applications in the study of ETS exposures, cancer prevention and tobacco product legislation. Our article is a review of the literature on smoking‐related adducts in human tissues published since 2002.

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Section: Exposure To Etsmentioning

confidence: 98%

“…45 Nonsmoking mothers exposed to ETS during pregnancy had detectable levels of HPB-releasing hemoglobin adducts, as did the fetal cord blood samples analyzed. 198…”

Section: Exposure To Etsmentioning

confidence: 99%

DNA and protein adducts in human tissues resulting from exposure to tobacco smoke

Phillips

Venitt

2012

Intl Journal of Cancer

124

122

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“…Hemoglobin, in the red cell, has a lifetime in the circulation of approximately 120 days. Therefore, levels of hemoglobin adduct will accumulate in the circulation, thereby enhancing the detection of the adduct and allowing its use as a biomonitor of exposure to various agents, such as those carcinogens found in tobacco smoke (65,68,(76)(77)(78)(79).…”

Section: Introduction Tobacco Exposure and Pregnancymentioning

confidence: 99%

The Relationship between Maternal and Fetal CYP1A1 Genotype in Smokers and Nonsmokers to Benzo(a)pyrene Hemoglobin Adducts

Myers

Barnes

Wright

et al. 2010

Polycyclic Aromatic Compounds

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Numerous methods exist by which we can follow exposure to tobacco smoke in experimental animals as well as in human populations. The simplest method to follow tobacco exposure is by assessing either urinary or serum cotinine levels. Although this provides an accurate assessment of short-term exposure to tobacco, it fails to provide a loan term assessment of exposure over several weeks and/or months. DNA adducts also provide effective means of monitoring exposure to tobacco smoke carcinogens. However, with the use of DNA adducts one deals with repair mechanisms, which may be altered as a result of the initial exposures. The ideal biomarker for use in assessing chemical exposures over a long-term basis is the use of the red cell protein hemoglobin. Formation of electrophilic metabolites of carcinogens has been shown to react with a variety of nucleophilic sites on hemoglobin, therefore forming covalent adducts which persists for the life of the red cell (120 days) and thus can be detected in used as a biomarker of exposure. Tobacco carcinogens must first be activated by a variety of enzymes prior to becoming electrophilic intermediates. Metabolic activation of these compounds proceeds by a number of steps, including the activation via cytochrome enzymes (CYP). Following activation of the carcinogens to a reactive electrophile, the reactive compound can form covalent adducts with DNA and protein. Following activation of the carcinogens, enzymes also are responsible for the detoxification of the reactive electrophilic metabolites. These enzymes help the body handle exposure to these compounds by facilitating detoxification and illumination of those reactive carcinogenic derivatives. The present study examined the relationship between polymorphism of CYP1A1 pharmacogenetics

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“…It has been established from numerous studies that cigarette smoke contains more than 40 known or putative carcinogens. 6 A direct association between cigarette smoking and various types of lung cancer has been observed for measures of intensity, duration, and dose. 7 To date, several polymorphisms in the wild-type p53 gene locus have been described.…”

Section: Introductionmentioning

confidence: 99%

Study of p53 codon 72 polymorphism and codon 249 mutations in Southern India in relation to age, alcohol drinking and smoking habits

et al. 2009

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Germline polymorphisms of genes involved in different steps of tumorigenesis like p53, the tumor suppressor gene, are reported to determine the individual susceptibility to cancer. Lung cancer is one of the most common and lethal cancers and tobacco smoking remains its most important etiologic factors. The most frequently p53 mutated codons of lung cancer are 72 (exon 4) and 249 (exon 7). Since mutations in the p53 gene are present in ∼40% of all human lung cancers and are more common in smokers than in nonsmokers, we aimed to detect the status of p53 at codon 72 for Arg/Arg or Arg/Pro or Pro/Pro allele polymorphism and p53 codon 249 mutation in smokers and nonsmokers of South India. Allele frequencies in the nonsmokers were 0.16 for the Arg/Pro allele and 0.84 for the Pro/Pro allele in our study population. Among the smokers, the frequencies of the Arg/Pro, Arg/Arg, and Pro/Pro alleles were 0.88, 0.04, and 0.08, respectively. No mutation was detected in both smokers and nonsmokers in p53 codon 249. From the worldwide scenario, it can be speculated that the smokers, with Arg/Pro genotype are more prone for lung cancer or to other types of cancer.

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Determination of Tobacco Specific Hemoglobin Adducts in Smoking Mothers and New Born Babies by Mass Spectrometry

Cited by 11 publications

References 68 publications

DNA and protein adducts in human tissues resulting from exposure to tobacco smoke

DNA and protein adducts in human tissues resulting from exposure to tobacco smoke

The Relationship between Maternal and Fetal CYP1A1 Genotype in Smokers and Nonsmokers to Benzo(a)pyrene Hemoglobin Adducts

Study of p53 codon 72 polymorphism and codon 249 mutations in Southern India in relation to age, alcohol drinking and smoking habits

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