DNA repair genes polymorphisms and damages induced by lead – a literature review
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Instytut Medycyny Pracy i Zdrowia Środowiskowego. Dyrektor: dr n. med. P. Z. Brewczyński
Elżbieta Olewińska   

Pracownia Toksykologii Genetycznej Instytut Medycyny Pracy i Zdrowia Środowiskowego ul. Kościelna 13; 41-200 Sosnowiec tel. 32 266 08 85; fax. 32 266 11 24
Med Srod. 2014;17(2):69–74
Lead is a toxic metal, which due to its superb properties is used in many industries. Due to the wide spectrum of its effects to human body it is very important to enhance the knowledge on the mechanisms of lead’s toxicity as well as to identify genetic determinants of defense against the harmful effects. DNA repair is one of the most important defense mechanisms against damage induced by lead. Gene polymorphisms may influence the recovery rate and recovery efficiency, and thus shape the individual susceptibility to lead exposure.
Ahamed M., Siddiqui M.K.J.: Low level lead exposure and oxidative stress: current opinions. Clin Chim Acta Int J Clin Chem 2007; 383: 57-64.
Patrick L.: Lead toxicity, a review of the literature. Part 1: Exposure, evaluation, and treatment. Altern Med Rev J Clin Ther 2006; 11: 2-22.
Bilban M.: Influence of the work environment in a Pb-Zn mine on the incidence of cytogenetic damage in miners. Am J Ind Med 1998; 34: 455-463.
Vaglenov A., Carbonell E., Marcos R.: Biomonitoring of workers exposed to lead. Genotoxic effects, its modulation by polyvitamin treatment and evaluation of the induced radioresistance. Mutat Res 1998; 418: 79-92.
Huang X.P., Feng Z.Y., Zhai W.L. i wsp.: Chromosomal aberrations and sister chromatid exchanges in workers exposed to lead. Biomed Environ Sci BES 1988; 1: 382-387.
Danadevi K., Rozati R., Saleha Banu B., i wsp.: DNA damage in workers exposed to lead using comet assay. Toxicology 2003; 187: 183-193.
Olewińska E., Kasperczyk A., Kapka L. i wsp.: Level of DNA damage in lead-exposed workers. Ann Agric Environ Med 2010; 17: 231-236.
Ye X.B., Fu H., Zhu J.L. i wsp.: A study on oxidative stress in lead-exposed workers. J Toxicol Environ Health A 1999; 57: 161-172.
Restrepo H.G., Sicard D., Torres M.M.: DNA damage and repair in cells of lead exposed people. Am J Ind Med 2000; 38: 330-334.
Chen Z., Lou J., Chen S.i wsp.: Evaluating the genotoxic effects of workers exposed to lead using micronucleus assay, comet assay and TCR gene mutation test. Toxicology 2006; 223: 219-226.
García-Lestón J., Roma-Torres.J, Vilares M. i wsp.: Biomonitoring of a population of Portuguese workers exposed to lead. Mutat Res 2011; 721: 81-88.
Wetmur J.G., Kaya A.H., Plewinska M. i wsp.: Molecular characterization of the human delta-aminolevulinate dehydratase 2 (ALAD2) allele: implications for molecular screening of individuals for genetic susceptibility to lead poisoning. Am J Hum Genet 1991; 49: 757-763.
Kelada S.N., Shelton E., Kaufmann R.B. i wsp.: Delta-aminolevulinic acid dehydratase genotype and lead toxicity: a HuGE review. Am J Epidemiol 2001; 154: 1-13.
Pawlas N., Olewińska E., Kozłowska A. i wsp.: Wpływ polimorfizmów genetycznych i interakcji gen-środowisko w ocenie skutków zdrowotnych środowiskowej i zawodowej ekspozycji na ołów – wybrane aspekty. Med Śr – Environ Med 2010; 13: 75-80.
Flora S.J.S., Mittal M., Mehta A.: Heavy metal induced oxidative stress & its possible reversal by chelation therapy. Indian J Med Res 2008; 128: 501-523.
Bartosz G.: Druga twarz tlenu. Wydawnictwo Naukowe PWN, Warszawa, 2008.
Valko M., Rhodes C.J., Moncol J. i wsp: Free radicals, metals and antioxidants in oxidative stress-induced cancer. Chem Biol Interact 2006; 160: 1-40.
Mohammad I.K., Mahdi A.A., Raviraja A. i wsp.: Oxidative stress in painters exposed to low lead levels. Arh Hig Rada Toksikol 2008; 59: 161-169.
Powell C.L., Swenberg J.A., Rusyn I.: Expression of base excision DNA repair genes as a biomarker of oxidative DNA damage. Cancer Lett 2005; 229: 1-11.
Schärer O.D.: Chemistry and biology of DNA repair. Angew Chem Int Ed Engl 2003; 42: 2946-2974.
Cooke M.S., Evans M.D., Dizdaroglu M. i wsp.: Oxidative DNA damage: mechanisms, mutation, and disease. FASEB J 2003; 17: 1195-1214.
De Vizcaya-Ruiz A., Barbier O., Ruiz-Ramos R. i wsp.: Biomarkers of oxidative stress and damage in human populations exposed to arsenic. Mutat Res 2009; 674: 85-92.
Roszkowski K.: Mechanizmy naprawy oksydacyjnych uszkodzeń DNA. Współczesna Onkol 2002; 6: 360-365.
McNeill D.R., Narayana A., Wong H-K. i wsp.: Inhibition of Ape1 nuclease activity by lead, iron, and cadmium. Environ Health Perspect 2004; 112: 799-804.
Hadi M.Z., Coleman M.A., Fidelis K. i wsp.: Functional characterization of Ape1 variants identified in the human population. Nucleic Acids Res 2000; 28: 3871-3879.
García-Lestón J., Roma-Torres J., Vilares M. i wsp.: Genotoxic effects of occupational exposure to lead and influence of polymorphisms in genes involved in lead toxicokinetics and in DNA repair. Environ Int 2012; 43: 29-36.
Janssen K., Schlink K., Götte W. i wsp.: DNA repair activity of 8-oxoguanine DNA glycosylase 1 (OGG1) in human lymphocytes is not dependent on genetic polymorphism Ser326/Cys326. Mutat Res 2001; 486: 207-216.
Andreassi M.G., Foffa I., Manfredi S. i wsp.: Genetic polymorphisms in XRCC1, OGG1, APE1 and XRCC3 DNA repair genes, ionizing radiation exposure and chromosomal DNA damage in interventional cardiologists. Mutat Res 2009; 666: 57-63.
Shen M.R., Zdzienicka M.Z., Mohrenweiser H. i wsp.: Mutations in hamster single-strand break repair gene XRCC1 causing defective DNA repair. Nucleic Acids Res 1998; 26: 1032-1037.
Lu C., He X., Yang Z.: Study on Relationship Between Gene Polymorphism of XRCC1 and Susceptibility to Lead Poisoning. Med J Commun 2006; Article_en/CJFDTOTAL-JTYX200604007.htm.
Liu X., Zhang Z.: Relationship between XRCC3 gene polymorphism and susceptibility to lead poisoning in male leadexposed workers. Chin J Ind Hyg Occup Dis 2013; 31: 401- 404.