Free radicals of benzo(a)pyrene and derivatives.

Sullivan, Paul D.

doi:10.1289/ehp.8564288

Cited by 11 publications

(9 citation statements)

References 51 publications

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“…DEPs and their extracts both seem to trigger signal transduction pathways involving ROS because the secretion of GM-CSF is strongly decreased after treatment with NAC. Indeed, polycyclic aromatic hydrocarbons such as benzo-[a]pyrene and 1-nitropyrene (23,35) as well as the activation of cytochrome P-450 have been shown to induce the production of ROS. We have shown that the increase in GM-CSF after DEP treatment is inhibited by the radical scavengers NAC, DMTU, and PDTC.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of GM-CSF increase by diesel exhaust particles in human airway epithelial cells

Boland

Bonvallot

Fournier

et al. 2000

American Journal of Physiology-Lung Cellular and Molecular Phys

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We have previously shown that exposure to diesel exhaust particles (DEPs) stimulates human airway epithelial cells to secrete the inflammatory cytokines interleukin-8, interleukin-1beta, and granulocyte-macrophage colony-stimulating factor (GM-CSF) involved in allergic diseases. In the present paper, we studied the mechanisms underlying the increase in GM-CSF release elicited by DEPs using the human bronchial epithelial cell line 16HBE14o-. RT-PCR analysis has shown an increase in GM-CSF mRNA levels after DEP treatments. Comparison of the effects of DEPs, extracted DEPs, or extracts of DEPs has shown that the increase in GM-CSF release is mainly due to the adsorbed organic compounds and not to the metals present on the DEP surface because the metal chelator desferrioxamine had no inhibitory effect. Furthermore, radical scavengers inhibited the DEP-induced GM-CSF release, showing involvement of reactive oxygen species in this response. Moreover genistein, a tyrosine kinase inhibitor, abrogated the effects of DEPs on GM-CSF release, whereas protein kinase (PK) C, PKA, cyclooxygenase, or lipoxygenase inhibitors had no effect. PD-98059, an inhibitor of mitogen-activated protein kinase, diminished the effects of DEPs, whereas SB-203580, an inhibitor of p38 mitogen-activated protein kinase, had a lower effect, and DEPs did actually increase the active, phosphorylated form of the extracellular signal-regulated kinase as shown by Western blotting. In addition, cytochalasin D, which inhibits the phagocytosis of DEPs, reduced the increase in GM-CSF release after DEP treatment. Together, these data suggest that the increase in GM-CSF release is mainly due to the adsorbed organic compounds and that the effect of native DEPs requires endocytosis of the particles. Reactive oxygen species and tyrosine kinase(s) may be involved in the DEP-triggered signaling of the GM-CSF response.

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Section: Discussionmentioning

confidence: 99%

Mechanisms of GM-CSF increase by diesel exhaust particles in human airway epithelial cells

Boland

Bonvallot

Fournier

et al. 2000

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Phenolic metabolites are also formed by direct hydroxylation at position C‐3 and C‐6 []. 6‐OH‐BaP undergoes one‐electron oxidation in the presence of peroxidases or cytochrome P450 to the toxic radical cation 6‐oxy‐BaP that is further oxidized to 1,6‐, 3,6‐, or 6,12‐quinones via hydroquinone and semiquinone radicals []. Quinones themselves are not mutagenic, but the reactive oxygen species generated by these intermediates are responsible for cytotoxic effects [].…”

Section: Metabolism and Molecular Toxicity Of Bapmentioning

confidence: 99%

Review on proteomic analyses of benzo[a]pyrene toxicity

et al. 2012

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Benzo[a]pyrene (BaP), a five-ring polycyclic aromatic hydrocarbon, is a well-recognized environmental pollutant. Coal-processing waste products, petroleum sludge, asphalt, creosote, and tobacco smoke, all contain high levels of BaP. Exposure to BaP elicits many adverse biological effects, including tumor formation, immunosuppression, teratogenicity, and hormonal effects. In addition to the genetic damage caused by BaP exposure, several studies have indicated the disruption of protein-protein signaling pathways. However, contrary to the large number of studies on BaP-induced DNA damage, only few data have been gathered on its effects at the protein level. This review highlights all proteomic studies to date used for assessing the toxicity of BaP and its metabolites in various organ systems. It will also give an overview on the role proteomics may play to elucidate the mechanisms underlying BaP toxicity.

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“…This may be explained by known properties of the chemicals. nC60 is an exceptional free radical scavenger [103,104], while B[a]P has been shown to produce free radicals under a variety of conditions [105]. reported on a loss in mitochondrial membrane potential in a mouse in vitro model, in association with increase in cellular ROS suggesting mitochondria associated apoptosis [107].…”

Section: Protein Expression Profilesmentioning

confidence: 99%

Antagonistic Interactions between Benzo[a]pyrene and C<sub>60</sub> in Toxicological Response of Marine Mussels

Barranger¹,

Langan²,

Sharma³

et al. 2019

Preprint

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This study aimed to assess the ecotoxicological effects of the interaction of fullerene (C60) and benzo[a]pyrene (B[a]P) on the marine mussel, Mytilus galloprovincialis. The uptake of nC60, B[a]P and mixtures of nC60 and B[a]P into tissues was confirmed by GC-MS, LC-HRMS and ICP-MS. Biomarkers of DNA damage as well as proteomics analysis were applied to unravel the toxic effect of B[a]P and C60. Antagonistic responses were observed at the genotoxic and proteomic level. Differentially expressed proteins (DEPs) were only identified in the B[a]P single exposure and the B[a]P mixture exposure groups containing 1 mg/L of C60, the majority of which were down-regulated (~52%). No DEPs were identified at any of the concentrations of nC60 (p < 0.05, 1% FDR). Using DEPs identified at a threshold of (p < 0.05; B[a]P and B[a]P mixture with nC60), gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) pathway analysis indicated that these proteins were enriched with a broad spectrum of biological processes and pathways, including those broadly associated with protein processing, cellular processes and environmental information processing. Among those significantly enriched pathways, the ribosome was consistently the top enriched term irrespective of treatment or concentration and plays an important role as the site of biological protein synthesis and translation. Our results demonstrate the complex multi-modal response to environmental stressors in M. galloprovincialis.

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Free radicals of benzo(a)pyrene and derivatives.

Abstract: The evidence for biological involvement, the spectroscopic properties (especially EPR), and the reactions, of free radicals derived from benzo(a)pyrene and its methylated, hydroxylated, and fluorinated derivatives are reviewed.

Cited by 11 publications

References 51 publications

Mechanisms of GM-CSF increase by diesel exhaust particles in human airway epithelial cells

Mechanisms of GM-CSF increase by diesel exhaust particles in human airway epithelial cells

Review on proteomic analyses of benzo[a]pyrene toxicity

Antagonistic Interactions between Benzo[a]pyrene and C<sub>60</sub> in Toxicological Response of Marine Mussels

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