Received on August 25, 2004
Accepted on January 21, 2005

General Clinical Chemistry

Increased Oxidative DNA Damage, as Assessed by Urinary 8-Hydroxy-2'-Deoxyguanosine Concentrations, and Serum Redox Status in Persons Exposed to Mercury

¹ Key Laboratory of Nuclear Analytical Techniques and Laboratory for Nanoscale Materials and Related Bio-Environmental Sciences, Institute of High Energy Physics, Chinese Academy of Sciences, Beijing, Peoples Republic of China
² Guizhou Research and Designing Institute of Environmental Sciences, Guiyang, Peoples Republic of China
³ School of Public Health, Peking University Health Science Center, Beijing, Peoples Republic of China
⁴ Department of Clinical Laboratory, Third Hospital of Peking University, Beijing, Peoples Republic of China

^* To whom correspondence should be addressed. E-mail: chenchy{at}mail.ihep.ac.cn.

Background: Mercury is a ubiquitous and highly toxic environmental pollutant. In this study, we evaluated the relationship between mercury exposure and oxidative stress, serum and urinary mercury concentrations, oxidative DNA damage, and serum redox status in chronically mercury-exposed persons compared with healthy controls.

Methods: We measured urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG), which we used as a biomarker of oxidative DNA damage, among the mercury-exposed persons, by HPLC with electrochemical detection (ECD). We evaluated antioxidant status by measuring the activities of superoxide dismutase and glutathione peroxidase and the concentrations of total reduced glutathione and protein-bound thiols in serum.

Results: The significant increase in 8-OHdG concentrations in urine indicated that mercury-induced oxidative damage to DNA occurred in vivo. Differences in body mercury burden and antioxidant enzyme activities were statistically significant between the mercury-exposed persons and controls. Serum and urinary mercury concentrations in the mercury-exposed persons were more than 40-fold higher than in controls.

Conclusions: Our data indicate that mercury exposure can induce oxidative DNA damage, whereas the antioxidative repair systems can be expected to minimize DNA lesions caused by mercury. In addition, our results suggest that measurement of urinary 8-OHdG could be useful for evaluating in vivo oxidative DNA damage in mercury-exposed populations.