Reprint of “In utero exposure to benzo[a]pyrene increases adiposity and causes hepatic steatosis in female mice, and glutathione deficiency is protective”

Ortíz, Laura Velasco; Nakamura, Brooke N.; Li, Xia; Blumberg, Bruce; Luderer, Ulrike

doi:10.1016/j.toxlet.2013.11.017

Cited by 14 publications

(6 citation statements)

References 70 publications

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“…4A), occurs in response to partial hepatectomy and also after chemical injury23. Exposure to benzo[a]pyrene (BaP), a model polycyclic aromatic hydrocarbon (PAH), leads to increased liver tumorigenesis24 and adiposity as well as hepatic steatosis25 in animals. Liver proliferation was identified in the top three most significantly affected mechanistic responses in Atlantic cod ( Gadus morhua ) larvae exposed to mechanically dispersed oil for four days26.…”

Section: Discussionmentioning

confidence: 99%

Novel transcriptome assembly and comparative toxicity pathway analysis in mahi-mahi (Coryphaena hippurus) embryos and larvae exposed to Deepwater Horizon oil

Mager

Grosell

et al. 2017

Sci Rep

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The impacts of Deepwater Horizon (DWH) oil on morphology and function during embryonic development have been documented for a number of fish species, including the economically and ecologically important pelagic species, mahi-mahi (Coryphaena hippurus). However, further investigations on molecular events and pathways responsible for developmental toxicity have been largely restricted due to the limited molecular data available for this species. We sought to establish the de novo transcriptomic database from the embryos and larvae of mahi-mahi exposed to water accommodated fractions (HEWAFs) of two DWH oil types (weathered and source oil), in an effort to advance our understanding of the molecular aspects involved during specific toxicity responses. By high throughput sequencing (HTS), we obtained the first de novo transcriptome of mahi-mahi, with 60,842 assembled transcripts and 30,518 BLAST hits. Among them, 2,345 genes were significantly regulated in 96hpf larvae after exposure to weathered oil. With comparative analysis to a reference-transcriptome-guided approach on gene ontology and tox-pathways, we confirmed the novel approach effective for exploring tox-pathways in non-model species, and also identified a list of co-expressed genes as potential biomarkers which will provide information for the construction of an Adverse Outcome Pathway which could be useful in Ecological Risk Assessments.

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Section: Discussionmentioning

confidence: 99%

Novel transcriptome assembly and comparative toxicity pathway analysis in mahi-mahi (Coryphaena hippurus) embryos and larvae exposed to Deepwater Horizon oil

Mager

Grosell

et al. 2017

Sci Rep

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“…High-molecular-weight PAHs, benzo[a]pyrene, impair adipose tissue lipolysis and lead to increased weight gain and increased fat mass and could have an impact on metabolic disorders, such as obesity [ 36 – 38 ]. Ortiz et al presented that early life exposure to tobacco smoke (containing PAHs) and air pollution (contaminated by PAHs) have been linked to increased risk of obesity and metabolic syndrome [ 35 , 39 ]. In addition, it has been recently discovered that PAHs may play a central role in carcinogenesis not only by inducing the cancer via their mutagenic properties, but also by enhanced bioaccumulation capacity of the adipose tissue [ 36 – 38 ].…”

Section: Discussionmentioning

confidence: 99%

Selected Inflammatory and Metabolic Markers in Psoriatic Patients Treated with Goeckerman Therapy

Kondělková

Borská

Andrýs

et al. 2015

Mediators of Inflammation

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Psoriasis is associated with metabolic activity of adipose tissue which produces pro- and anti-inflammatory adipokines. Goeckerman therapy (GT) represents an effective treatment of psoriasis. This study evaluated variation of selected inflammatory and metabolic markers during GT and the relationships between the markers, severity of the disease (PASI score), body mass, and the basic characteristics of the therapy. The study was conducted on a group of patients (n = 32) and on a control group (n = 24). Before GT, we found significantly elevated levels of proinflammatory CRP (p < 0.001) and leptin (p < 0.05) in psoriatic patients (compared to the controls). The therapy significantly decreased the levels of CRP and adiponectin. We found positive correlations between CRP and total duration of GT (p < 0.05) and CRP and the time of UV exposure (p < 0.01) and negative correlations between adiponectin and the total duration of GT (p < 0.05) and adiponectin and the application of CCT ointment (p < 0.001). From our results, we can conclude that GT causes partial reduction of both proinflammatory and anti-inflammatory markers. However, the levels of proinflammatory CRP and leptin remained significantly higher in the patients than in the control group.

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“…This well-recognized genotoxic carcinogen to humans is thus metabolized by the liver (see eg. 19 ), and has been suggested to induce liver steatosis 20 , 21 as well as hepatocellular carcinoma (HCC), especially in human 22 , 23 . Besides, epidemiological studies suggest a synergistic effect of B[a]P and alcohol on HCC risk 24 .…”

Section: Introductionmentioning

confidence: 99%

Co-exposure to benzo[a]pyrene and ethanol induces a pathological progression of liver steatosis in vitro and in vivo

Bucher

Tête

Podechard

et al. 2018

Sci Rep

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Hepatic steatosis (i.e. lipid accumulation) and steatohepatitis have been related to diverse etiologic factors, including alcohol, obesity, environmental pollutants. However, no study has so far analyzed how these different factors might interplay regarding the progression of liver diseases. The impact of the co-exposure to the environmental carcinogen benzo[a]pyrene (B[a]P) and the lifestyle-related hepatotoxicant ethanol, was thus tested on in vitro models of steatosis (human HepaRG cell line; hybrid human/rat WIF-B9 cell line), and on an in vivo model (obese zebrafish larvae). Steatosis was induced prior to chronic treatments (14, 5 or 7 days for HepaRG, WIF-B9 or zebrafish, respectively). Toxicity and inflammation were analyzed in all models; the impact of steatosis and ethanol towards B[a]P metabolism was studied in HepaRG cells. Cytotoxicity and expression of inflammation markers upon co-exposure were increased in all steatotic models, compared to non steatotic counterparts. A change of B[a]P metabolism with a decrease in detoxification was detected in HepaRG cells under these conditions. A prior steatosis therefore enhanced the toxicity of B[a]P/ethanol co-exposure in vitro and in vivo; such a co-exposure might favor the appearance of a steatohepatitis-like state, with the development of inflammation. These deleterious effects could be partly explained by B[a]P metabolism alterations.

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Reprint of “In utero exposure to benzo[a]pyrene increases adiposity and causes hepatic steatosis in female mice, and glutathione deficiency is protective”

Cited by 14 publications

References 70 publications

Novel transcriptome assembly and comparative toxicity pathway analysis in mahi-mahi (Coryphaena hippurus) embryos and larvae exposed to Deepwater Horizon oil

Novel transcriptome assembly and comparative toxicity pathway analysis in mahi-mahi (Coryphaena hippurus) embryos and larvae exposed to Deepwater Horizon oil

Selected Inflammatory and Metabolic Markers in Psoriatic Patients Treated with Goeckerman Therapy

Co-exposure to benzo[a]pyrene and ethanol induces a pathological progression of liver steatosis in vitro and in vivo

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