Oxidative DNA damages by chemical exposures at work

Abstract

ABSTRACTdiseases. 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.

Assessment of air quality and erythrocyte oxidative stress indicators of storekeepers of laboratory/industrial chemicals in owerri, Imo state, Nigeria

“…Biological and epidemiological studies have provided evidence in support of the fact that toxic air pollutants are among the major underlying causative factors of oxidative stress [10] . According to Agrawal and Sharma [11] , pesticides induced oxidative stress in mammalian systems was the outcome of distortions in the balance between tissue ROS and antioxidant levels, which engendered tissue damage to onset of several pathologic challenges and finally apoptosis.…”