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Chrysene is a four-ring polycyclic aromatic hydrocarbon, which has been demonstrated to induce adverse effects through the inducement of oxidative stress. However, the possible mechanisms and potential pathways of chrysene-induced oxidative damages are scarcely investigated. In the present study, oxidative stress and xenobiotic metabolism disorder were investigated in human hepatocytes. Chrysene could cause cell viability reduction and cellular reactive oxygen species accumulation in a dose-dependent manner from 10 to 400 ng/mL. Moreover, the mRNA expression detoxification phases, including phase I and phase II as xenobiotic metabolizing enzymes, along with phase III, were investigated by real-time PCR. The results showed that chrysene upregulated the phase I enzymes cytochrome P-450 1A1, 1A2, and epoxide hydrolase 1, while at the same time downregulated the phase II enzymes glutathione S-transferase alpha 1, NAD(P)H: quinone oxidoreductase 1, and the phase III transporters multiple drug resistant 1 and multidrug resistance-associated protein 2. Furthermore, the inflammatory markers tumor necrosis factor alpha, interleukin-6, interleukin-8, and cyclooxygenase-2 were increased, whereas the antioxidant transcription factor nuclear factor erythroid 2-related factor 2 and its regulated enzymes glutathione peroxidase1, heme oxygenase-1, and superoxide dismutase 2 were decreased. These data suggested that chrysene expressed oxidative stress to hepatocytes, resulting in cytotoxicity and inflammation, which might be due to the damage of the antioxidant system and xenobiotic metabolism.

Adverse Effects of Chrysene on Human Hepatocytes via Inducement of Oxidative Stress and Dysregulation of Xenobiotic Metabolism