1887

Abstract

Abstract

Chronic exposure to environmental toxic chemicals can cause DNA damage, disease and strong selection pressure on the gene pool of exposed populations. A mechanism that can link the exposure and biological consequences is DNA repair activity. Therefore, impairment of the DNA repair function can be a critical mechanism for the development of environmental health problems. In my laboratory, we have developed a Challenge assay to detect functional DNA repair deficiencies. In this assay, lymphocytes from exposed and control subjects are irradiated with X-rays or UV-light to induce DNA damage, thus challenging them to repair the damage. Abnormal repair will result in significantly elevated chromosome aberrations or DNA strand breaks in the Comet assay. Studies around the world have used the assay to indicate that excessive exposure to mutagenic and toxic substances can cause abnormal DNA repair responses. Thus, the risk for the development of health problems is increased. In studies in collaboration with Professor Bersimbaev of Kazakhstan, 3 generations of residents who have been exposed to radioactive fallouts from nuclear bomb testings were studied. The population had generation-based increase in mini-satellite instability and preferential retention of the GSTM1 null genotype. It appears that the chronic exposure to ionizing radiation has caused DNA repair defects and the alteration of the gene pool. The latter suggests that selection pressure can potentially alter the genetic makeup of the future generations. However, no clear cut evidence of such exists among exposed human populations. In summary, these studies indicate that excessive exposure to hazardous substances can cause functional alterations in the DNA repair machinery leading to increase health risk, including the possibility of alteration of gene pool in exposed population

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/content/papers/10.5339/qproc.2012.mutagens.3.14
2012-03-01
2019-10-22
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http://instance.metastore.ingenta.com/content/papers/10.5339/qproc.2012.mutagens.3.14
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  • Received: 07 May 2012
  • Accepted: 07 May 2012
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