Oxidative DNA damages by chemical exposures at work

diseases. These include cancer, Parkinson’s disease, Alzheimer’s disease, atherosclerosis, heart failure, myocardial infarction, Schizophrenia, bipolar disorder, fragile X syndrome, sickle cell disease and chronic fatigue syndrome. Oxidative stress is likely to be involved in agerelated development of cancer. The reactive species produced in oxidative stress can cause direct damage to the DNA and are therefore mutagenic, and it may also suppress apoptosis and promote proliferation, invasiveness and metastasis [1]. Oxidative DNA damage is an inevitable consequence of cellular metabolism, with a propensity for increased levels following toxic insult. Of the molecules subject to oxidative modification, DNA has received the greatest attention, with biomarkers of exposure and effect closest to validation. There are many chemicals in workplaces that could cause oxidative DNA damages such as carcinogens. This review concentrated on studies published between the years 2000 and 2012 that used to detect 8-oxodG in humans (workers), laboratory animals and in cell lines. Given the recent toxicological results from oxidative stress, it is important to review these studies to improve the current understanding of the oxidative DNA damages by chemical exposures at work. It also suggests that biomarkers may be responsible for understanding the role of oxidative DNA damage in disease, highlighting the need for further studies. The presence of metals in biological systems in an uncomplexed form (not in a protein or other protective metal complex) can significantly increase the level of oxidative stress. The major portion of long term effects is inflicted by damage on DNA. Some of the less reactive of these species (such as superoxide) can be converted by oxidoreduction reactions with transition metals or other redox cycling compounds (including quinones) into more aggressive radical species that can cause extensive cellular damage. Disturbances in the normal redox state of cells can cause toxic effects through the production of peroxides and free radicals that damage all components of the cell, including proteins, lipids, and DNA. Further, some reactive oxidative species act as cellular messengers in redox signaling. Thus, oxidative stress can cause disruptions in normal mechanisms of cellular signaling. Metals such as iron, copper, chromium, vanadium and cobalt are capable of redox cycling in which a single electron may be accepted or donated by the metal. Most important reactions are probably Fenton’s reaction and the Haber-Weiss reaction, in which hydroxyl radical is produced from reduced iron and hydrogen peroxide. The presence of such metals in biological systems in an uncomplexed form (not in a protein or other protective metal complex) can significantly increase the level of oxidative stress. In humans, hemochromatosis is associated with increased tissue iron levels, Wilson’s disease with increased tissue levels of copper and chronic manganism with exposure to manganese ores. The reaction of transition metals with proteins oxidated by reactive oxygen species can yield reactive products that accumulate with time and contribute to aging and disease [2].