Alkylated polycyclic aromatic compounds (alkyl-PACs) are the major aromatic constituent of total PAH in crude oil and originated from incomplete combustion process. Whereas benzo[a]pyrene (BaP) is a well-known human carcinogen, dibenzothiophene (DBT) and retene (Ret) are not; however, all three compounds are important environmental pollutants. Their toxicity is not yet characterized. In this study, we used BaP (parent PAH), DBT and Ret (alkyl-PACs) to elucidate the mechanism of neurotoxicity using human neuroblastoma cells. The lethal concentrations (LC10 & LC20) were found at around 10 µM and 40 µM after 24 hours exposer to SK-N-SH cells. Exposed differentiated neuronal cells showed significant dose-dependent increase levels of reactive oxygen species (ROS), even at with sub-lethal concentration (DBT, and
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2001). It has been suggested that effects of ROS on human cells may induce the oxidative injury leading to apoptosis (Salganik 2001). To study the relationship between ROS production and apoptosis, BaP-, DBT-, and Ret-induced ROS production in SK-N-SH cells was measured following exposure to CM-H2DCFDA, which forms a fluorescent oxidation product in the presence of ROS. Fig. ….shows the ROS levels after exposure to BaP, DBT, Ret, and H2O2 (positive control). A dose-dependent significant increase was detected in cells exposed to LC10, and LC20 treatments. To elucidate the type of ROS, we measured the intracellular and mitochondrial ROS. There were no significant intracellular H2O2 productions, but the mitochondrial ROS levels (superoxide production) were significantly increased by the exposure of BaP, DBT, and Ret (Fig….). Mitochondria are an important source of ROS, and the mitochondrial oxidative stress leads to many pathologies (Murphy 2009). Thus, BaP, DBT, and Ret trigger the formation of mitochondrial ROS in differentiated SK-N-SH cells, leading to
2001). It has been suggested that effects of ROS on human cells may induce the oxidative injury leading to apoptosis (Salganik 2001). To study the relationship between ROS production and apoptosis, BaP-, DBT-, and Ret-induced ROS production in SK-N-SH cells was measured following exposure to CM-H2DCFDA, which forms a fluorescent oxidation product in the presence of ROS. Fig. ….shows the ROS levels after exposure to BaP, DBT, Ret, and H2O2 (positive control). A dose-dependent significant increase was detected in cells exposed to LC10, and LC20 treatments. To elucidate the type of ROS, we measured the intracellular and mitochondrial ROS. There were no significant intracellular H2O2 productions, but the mitochondrial ROS levels (superoxide production) were significantly increased by the exposure of BaP, DBT, and Ret (Fig….). Mitochondria are an important source of ROS, and the mitochondrial oxidative stress leads to many pathologies (Murphy 2009). Thus, BaP, DBT, and Ret trigger the formation of mitochondrial ROS in differentiated SK-N-SH cells, leading to