8 Hydroxydeoxyguanosine as a biomarker of workplace exposures

Abstract

To date, the 8-hydroxydeoxyguanosine (8OHdG) DNA adduct has been used as a biomarker in 11 occupational health studies examining the potential for ten different workplace exposures to cause oxidative DNA damage. Exposures examined include asbestos, azo-dyes, benzene, chromium, coal dust, glassworks, rubber manufacturing, styrene, toluene and environmental tobacco smoke (ETS). Experimental designs that applied 8OHdG as biomarker varied dramatically among the studies. For example, one study detected increased urinary excretion in retired workers with a history of exposure to mining dusts, while a study of workers exposed to benzene showed that the pattern of urinary excretion of 8OHdG varied over a 24h period following exposure. All but one study reported increased 8OHdG relative to controls, but in three cases the increases were not statistically significant. Only one study demonstrated a dose-response relationship between a chemical exposure (benzene) in the workplace and elevated 8OHdG. In most cases, exposure data were lacking and the elevated 8OHdG could only be considered to be associated with a generalized job category. Numerous animal and human studies have demonstrated an effect of tobacco smoke on 8OHdG, including a study of ETS in the workplace. In the majority of occupational studies, however, smoking was found not to be a confounding variable. 8OHdG levels tended to be higher in women than men as did the response to an occupational exposure and/or smoking. Two of three studies that stratified workers by age found it to be a confounder for the 8OHdG adduct, but the relationship between age and 8OHdG was non-linear. Only one study considered the impact of dietary supplements on 8OHdG levels in workers despite the fact that diet can have a marked effect on an individual's response to oxidative stress. It is premature to consider 8OHdG as biomarker that can be used for decision making or for regulatory purposes. Nonetheless, these studies demonstrate that with additional characterization of the role 8OHdG plays in the exposure-disease continuum it may well serve as a powerful biomonitoring toolin the future.

Increase of urinary concentrations of 8-hydroxy-2′-deoxyguanosine in diesel exhaust emission inspector exposed to polycyclic aromatic hydrocarbons

“…One study even reported an insignificant negative association between smoking and urinary 8-OHdG levels (Nilsson et al 2004). Many occupational studies did not find higher concentrations of 8-OHdG in smokers even though smoking has consistently been recognized to be a cofounder for 8-OHdG (Angerer et al 2007;Pilger and Rüdiger 2006;Toraason 1999). Regardless, smoking is a factor that should not be ignored.…”

Analysis of aromatic DNA adducts and 7,8-dihydro-8-oxo- 2′-deoxyguanosine in lymphocyte DNA from a case–control study of lung cancer involving minority populations

“…Higher levels of 8-oxo-dG have been detected in a central site in the lungs of cigarette smokers, and a positive association between 8-oxo-dG levels in lung tissue and the Brinkman index (cigarettes/day  years) obtained from smokers and exsmokers has been reported [63]. Also, lymphocytes have been used as a surrogate tissue to detect 8-oxo-dG from smokers and nonsmokers [25,64]. Consistent with the above observations, we detected signi®cantly higher levels of 8-oxo-dG in lymphocyte DNA of lung cancer cases than of corresponding controls, who were predominantly current smokers ( Figure 3B and Table 3).…”

“…Thus, observations from clinical studies [24,25,29] and the data in this study suggest a causal role for smoking-related free radicals in lung carcinogenesis. Very few studies have considered sex in the assessment of chemically induced oxidative DNA damage [64]. In a study of benzeneexposed workers, Liu et al [65] found signi®cantly higher levels of 8-oxo-dG in lymphocyte DNA in women versus men, however, no gender-dependent differences in oxidative DNA damage was observed between controls.…”

Alterations of Mitochondrial Functions and DNA in Diabetic Cardiomyopathy of CCK1 Receptors-Deficient Rats

“…The significant increase of 8-OHdG level in mitochondrial DNA of diabetic heart ( Figure 6) indicated the oxidative damage of DNA leading to diabetic cardiomyopathy. This is where 8-OH-dG can be considered as a promutagenic lesion in DNA that is generated in response to a number of chemicals that induce oxidative stress [33] and it is widely used as a marker of oxidative injury [34].…”