Analysis of Halogenated Polycyclic Aromatic Hydrocarbons in the Air

Ohura, Takeshi; Kamiya, Yuta; Ikemori, Fumikazu; Ando, Masanori

doi:10.5772/48720

Cited by 1 publication

(1 citation statement)

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“…Even though water contamination by PAHs has not been well exploited, it is of equal or greater importance to study the presence and the harmful effects of PAHs in this indispensable resource for all living organisms. In fact, the presence of these compounds in freshwater that may be captured for human use and consumption is a serious problem because the conventional water‐treatment processes (such as coagulation or filtration) do not guarantee their complete removal . Concern with human exposure to PAHs by drinking‐water consumption was expressed by the World Health Organization based on the toxicity of the individual compounds identified and the total PAH dose ingested per day .…”

Section: Introductionmentioning

confidence: 99%

Integration of cellular and molecular endpoints to assess the toxicity of polycyclic aromatic hydrocarbons in HepG2 cell line

Morgado¹,

José²,

Wanke

et al. 2017

Environmental Toxicology and Chemistry

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Polycyclic aromatic hydrocarbons (PAHs) are persistent pollutants present in the environment with known mutagenic and carcinogenic properties. In the present study the effects of exposure to single or multiple doses of benzo[a]anthracene (BaA), pyrene (Pyr), and 3 halogenated derivatives of these compounds (1-chloropyrene, 1-bromopyrene [1-BrPyr], and 7-chlorobenzo[a]anthracene [7-ClBaA]) were evaluated in a liver-derived human cell line (HepG2). Cytotoxicity as assessed by the classic 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and neutral red assays showed a mild toxic effect in response to single or multiple dose exposure for up to 72 h, except for multiple dose exposure to BaA and 7-ClBaA (1 μM/d for 4 d) and single exposure to 10 μM BaA. Furthermore, selective mitochondrial and lysosomal toxicity was observed for Pyr and BaA series, respectively. To understand the underlying molecular mechanisms responsible for this effect, reactive oxygen species production, mitochondrial membrane depolarization, lysosomal pH, DNA fragmentation, and early and late apoptosis mediators were evaluated after exposure to single doses of the compounds. All compounds were able to trigger oxidative stress after 24 h as measured by catalase activity, and a good correlation was found between mitochondrial membrane depolarization, lysosomal pH increase, and MTT and neutral red assays. Evaluation of cell death mediators showed that caspase-3/7, but not annexin-V, pathways were involved in toxicity triggered by the studied compounds. The integration of all results showed that 1-BrPyr and BaA have a higher toxicity potential. Environ Toxicol Chem 2017;36:3404-3414. © 2017 SETAC.

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Section: Introductionmentioning

confidence: 99%