Abstract

In this study, we investigated oxidative stress and tumor marker levels of polycyclic aromatic hydrocarbons (PAHs) in 136 coke oven workers and in 60 control subjects, and evaluated the correlation between oxidative stress and tumor marker levels. Questionnaires on basic demographic information were also administered. Significant differences in employment time and percentages of alcohol drinkers were observed between the control and exposed groups. PAH exposure was assessed using urinary 1-hydroxy-pyrene (1-OHP) levels and was found to be significantly higher in workers than in the controls. Significant differences (P<0.001) of MDA, GST, LDH, NSE, Cyfra21-1, and of SCC and TNF-a (P<0.0001 and P<0.05, P<0.001, respectively) levels were observed among controls and coke-oven workers, except for bottom coke oven workers. Associations between age and risk of increased TNF-a, smoking and increased GST activities, and drinking with increased MDA concentrations, were marginal (P=0.055, P=0.048, P=0.057, respectively). The association between smoking with MDA (P=0.004), NSE (P=0.005), SCC (P=0.004) and TNF-a (P<0.001), and drinking with TNF-a levels was significant (P=0.012). In addition, a significant positive correlation between oxidative stress and tumor markers was found in the present study. These results suggest that a synergistic increase of oxidative stress and tumor markers induced by PAHs may play a role in toxic responses for PAHs in coke oven workers.

Highlights

  • Polycyclic aromatic hydrocarbons (PAHs) are a complex mixture of chemicals and a well-established group of chemical carcinogens

  • These results suggest that a synergistic increase of oxidative stress and tumor markers induced by polycyclic aromatic hydrocarbons (PAHs) may play a role in toxic responses for PAHs in coke oven workers

  • We examined the serum tumor markers such as Cyfra21-1, squamous cell carcinoma antigen (SCC), neuron specific enolase (NSE) and Tumor necrosis factor (TNF)-a in PAHs exposure of coke-oven workers

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Summary

Introduction

Polycyclic aromatic hydrocarbons (PAHs) are a complex mixture of chemicals and a well-established group of chemical carcinogens. PAHs are metabolized by cytochrome P450 to diol epoxides capable of binding covalently to DNA, potentially initiating the carcinogenic process (Jongeneelen et al, 1987; Nerurkar et al, 2000). PAHs metabolites can be detoxified by GST and uridine diohospho glucuronosyltransferase, which catalyze conjugative reactions of oxidative products, including oxidative metabolites of 1-hydroxypyrene (1-OHP) and 3-hydroxybenzo[a]pyrene (3-OH-BaP). Reactive oxygen species including superoxide, H2O2, lOH and semiquinone radicals caused by PAHs further cause the excessive oxidative stress (Gao et al, 2010). Oxidative stress is defined as an impaired balance between free radical production and antioxidant capacity resulting in excess oxidative products (Hong et al, 2009). The generation of reactive oxygen species can cause oxidative damage to DNA, proteins, or lipids in the body. The generation of oxidative stress is indicated by lactate dehydrogenase (LDH) leakage (Yang et al, 2007)

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