A metabolomics strategy to assess the combined toxicity of polycyclic aromatic hydrocarbons (PAHs) and short-chain chlorinated paraffins (SCCPs)

Wang, Feidi; Zhang, Haijun; Geng, Ningbo; Ren, Xiaoqian; Zhang, Baoqin; Gong, Yufeng; Chen, Jiping

doi:10.1016/j.envpol.2017.11.073

Cited by 65 publications

(23 citation statements)

References 51 publications

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“…In the present study, content of inosine increased 1.53-fold in treatment with 9,10-PQ, compared with the control, indicating that T. obscurus may produce more inosine to resist oxidative stress and harmful effects on immunity caused by 9,10-PQ. Downregulation of guanosine in the present study was similar to a previous cell culture experiment, in which exposure to 160 µg l −1 PAHs mixture significantly downregulated the level of guanosine due to inhibition of hypoxanthine guanine phosphoribosyl transferase (HGPRT) [56,57]. Oxidation of guanosine is a biomarker of oxidative stress [58].…”

Section: Discussionsupporting

confidence: 89%

Effects of 9,10-phenanthrenequione on antioxidant indices and metabolite profiles in Takifugu obscurus plasma

2020

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Derived from polycyclic aromatic hydrocarbons (PAHs), oxygenated-PAHs (oxy-PAHs) may pose hazards to aquatic organisms, which remain largely unknown. Takifugu obscurus is an important anadromous fish species of high economic and ecological values. In the present study, T. obscurus was acutely exposed to 44.29 µg l −1 9,10-phenanthrenequione (9,10-PQ) for 96 h. Changes of antioxidant indices and metabolite profiles in plasma were compared between 9,10-PQ treatment and the control. The results showed that 9,10-PQ treatment significantly increased malondialdehyde (MDA) content during 6 to 96 h, increased superoxide dismutase (SOD) and catalase (CAT) activities at 6 h, but decreased them at 96 h. These results indicated that 9,10-PQ induced oxidative stress to fish. Ultra-performance liquid chromatography-mass spectrometry (UPLC-MS) analysis revealed that four metabolic pathways were influenced in response to treatment with 9,10-PQ, including glycerophospholipid metabolism, phenylalanine, tyrosine and tryptophan biosynthesis, purine metabolism and sulfur metabolism. These pathways are associated with antioxidant mechanisms, biosynthesis of neurotransmitters and innate immune functions. Thus, the as-obtained results confirmed that 9,10-PQ induced oxidative stress and raised concerns of neurotoxicity and immunotoxicity to fish. Overall, the present study posed a high environmental risk of oxy-PAHs to aquatic ecosystems.

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Section: Discussionsupporting

confidence: 89%

Effects of 9,10-phenanthrenequione on antioxidant indices and metabolite profiles in Takifugu obscurus plasma

2020

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“…4−7 Evidence has been found that combined human exposure to PAHs and SCCPs results in an additive effect on the overall metabolism. 31 Therefore, risk assessment should not only focus on the individual compounds present in the rubber, but should also address possible synergistic/additive effects.…”

Section: Resultsmentioning

confidence: 99%

Chlorinated Paraffins in Car Tires Recycled to Rubber Granulates and Playground Tiles

Brandsma

Brits

Groenewoud

et al. 2019

Environ. Sci. Technol.

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Chlorinated paraffins (CPs) are used in various products to improve their physicochemical characteristics. Due to recycling, CPs may end up in “new” recycled products. In this study we investigated CPs present in end-of-life car tires that are recycled to rubber granulates used on artificial soccer fields, and playground tiles. The ∑CP(C10-C30) concentrations ranged from 1.5 to 67 μg/g in car tires, 13–67 μg/g in rubber granulates, and 16–74 μg/g in playground tiles. MCCPs were the dominant CP group with an average contribution of 72%. LCCPs up to C30, were detected for the first time in car tires, rubber granulates, and playground tiles. The CPs application in tires is unclear, the low CP concentrations found in this study (<0.007%) could possibly indicate contamination during the manufacturing process. The presence of CPs in the granulates and tiles, in addition to the multiple chemicals already detected, emphasizes the need to further investigate the migration and leaching behavior, in order to assess potential risks of CPs for humans and the environment. The presence of CPs in car tires may be another source of CPs for the environment. The CP volume brought into the environment by tire wear particles (TWP) from car tires in the European Union, is estimated at 2.0–89 tons annually.

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“…In addition, the top PC identified in Figure 8 (PC 36:4) has also been specifically linked to AA production (Banno et al, 2017), providing further evidence in support of our findings herein. Phospholipids, such as PC, LysoPC, PE, and LysoPE, were upregulated in the HepG2 cell line exposed to PAHs and SCCP and analyzed via metabolomics methods (Wang et al, 2018). Polycyclic aromatic hydrocarbon exposure can also activate PLA 2 with fatty acid supplementation (Gdula-Argasi nska et al, 2016;Tithof et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Early Mechanistic Events Induced by Low Molecular Weight Polycyclic Aromatic Hydrocarbons in Mouse Lung Epithelial Cells: A Role for Eicosanoid Signaling

Siegrist

Romo

Upham

et al. 2019

Toxicological Sciences

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Low molecular weight polycyclic aromatic hydrocarbons (LMW PAHs; < 206.3 g/mol) are under regulated environmental contaminants (eg, secondhand smoke) that lead to gap junction dysregulation, p38 MAPK activation, and increased mRNA production of inflammatory mediators, such as cytokines and cyclooxygenase (COX2), in lung epithelial cells. However, the early mechanisms involving lipid signaling through the arachidonic acid pathway and subsequent eicosanoid production leading to these downstream events are not known. Common human exposures are to mixtures of LMW PAHs, thus C10 cells (a mouse lung epithelial cell line) were exposed to a representative binary PAH mixture, 1-methylanthracene (1-MeA) and fluoranthene (Flthn), for 30 min-24 h with and without p38 and cytosolic phospholipase A 2 (cPLA 2 ) inhibitors. Cytosolic phospholipase A 2 inhibition reversed PAH-induced phospho-p38 MAPK activation and gap junction dysregulation at 30 min. A significant biphasic increase in cPLA 2 protein was observed at 30 min, 2, and 4 h, as well as COX2 protein at 2 and 8 h. Untargeted metabolomics demonstrated a similar trend with significantly changing metabolites at 30 min and 4 h of exposure relative to 1 h; a "cPLA 2 -like" subset of metabolites within the biphasic response were predominately phospholipids. Targeted metabolomics showed several eicosanoids (eg, prostaglandin D 2 (PGD 2 ), PGE 2a ) were significantly increased at 4, 8, and 12 h following exposure to the binary PAH mixture and this effect was p38-dependent. Finally, PAH metabolism was not observed until after 8 h. These results indicate an early lipid signaling mechanism of LMW PAH toxicity in lung epithelial cells due to parent PAH compounds.

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A metabolomics strategy to assess the combined toxicity of polycyclic aromatic hydrocarbons (PAHs) and short-chain chlorinated paraffins (SCCPs)

Cited by 65 publications

References 51 publications

Effects of 9,10-phenanthrenequione on antioxidant indices and metabolite profiles in Takifugu obscurus plasma

Effects of 9,10-phenanthrenequione on antioxidant indices and metabolite profiles in Takifugu obscurus plasma

Chlorinated Paraffins in Car Tires Recycled to Rubber Granulates and Playground Tiles

Early Mechanistic Events Induced by Low Molecular Weight Polycyclic Aromatic Hydrocarbons in Mouse Lung Epithelial Cells: A Role for Eicosanoid Signaling

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