Early life co-exposures to a real-world PAH mixture and hypoxia result in later life and next generation consequences in medaka (Oryzias latipes)

Mu, Jingli; Chernick, Melissa; Wang, Dong; Giulio, Richard T. Di; Hinton, David E.

doi:10.1016/j.aquatox.2017.06.026

Cited by 19 publications

(8 citation statements)

References 108 publications

(167 reference statements)

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“…Sorption of NanoPS with PAHs for 7 days before the exposure period did not lead to acute toxicity or teratogenicity. The environmental mixture of PAHs used in this study (ERSE) is a potent inducer of cardiac toxicity in developing fish (Brown et al, 2016;Riley et al, 2016;Lindberg et al, 2017;Mu et al, 2017;Trevisan et al, 2019). The lack of such findings in animals exposed to PAH-NanoPS suggests, at least, two possible scenarios.…”

Section: Discussionmentioning

confidence: 88%

“…It was previously collected, processed, and chemically characterized by our laboratory with a total PAH content of 5,073 ng/mL PAHs as a result of 36 different analyzed PAHs (Fang et al, 2014). This solution has been extensively studied in our laboratory as a model environmental PAH mixture with different fish species, including zebrafish (D. rerio), Atlantic killifish (Fundulus heteroclitus) and medaka (Oryzias latipes) (Brown et al, 2016;Riley et al, 2016;Lindberg et al, 2017;Mu et al, 2017;Trevisan et al, 2019). This extract was obtained from sediments collected at the Atlantic Wood Industries Superfund Site (VA, United States), which contained 122.6 µg/g dry sediment of total PAHs (Clark et al, 2013).…”

Section: Plastic Nanoparticles and An Environmental Mixture Of Pahsmentioning

confidence: 99%

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PAH Sorption to Nanoplastics and the Trojan Horse Effect as Drivers of Mitochondrial Toxicity and PAH Localization in Zebrafish

Trevisan

Uzochukwu

Giulio

2020

Front. Environ. Sci.

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Plastics are world-wide pollutants that pose a potential threat to wildlife and human health. Small plastic particles, such as microplastics and nanoplastics, are easily ingested, and can act as a Trojan Horse by carrying microorganisms and pollutants. This study investigated the potential role of the Trojan Horse effect in the toxicity of nanoplastics to the vertebrate model organism, zebrafish (Danio rerio). First, we investigated if this effect could affect the toxicity of nanoplastics. Second, we analyzed if it could contribute to the biodistribution of the associated contaminants. And third, we focused on its effect on the mitochondrial toxicity of nanoplastics. We incubated 44 nm polystyrene nanoparticles with a real-world mixture of polycyclic aromatic hydrocarbons (PAHs) for 7 days and removed the free PAHs by ultrafiltration. We dosed embryos with 1 ppm of nanoplastics (NanoPS) or PAH-sorbed nanoplastics (PAH-NanoPS). Neither type of plastic particle caused changes in embryonic and larval development. Fluorescence microscopy and increased EROD activity suggested the uptake of PAHs in larvae exposed to PAH-NanoPS. This coincided with higher concentrations in the yolk sac and the brain. However, PAH-only exposure leads to their accumulation in the yolk sac but not in the brain, suggesting that that the spatial distribution of bioaccumulated PAHs can differ depending on their source of exposure. Both nanoplastic particles affected mitochondrial energy metabolism but caused different adverse effects. While NanoPS decreased NADH production, PAH-NanoPS decreased mitochondrial coupling efficiency and spare respiratory capacity. In summary, the addition of PAHs to the surface of nanoplastics did not translate into increased developmental toxicity. Low levels of PAHs were accumulated in the organisms, and the transfer of PAHs seems to happen in tissues and possibly organelles where nanoplastics accumulate. Disruption of the energy metabolism in the mitochondria may be a key factor in the toxicity of nanoplastics, and the Trojan Horse effect may amplify this effect.

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Section: Discussionmentioning

confidence: 88%

Section: Plastic Nanoparticles and An Environmental Mixture Of Pahsmentioning

confidence: 99%

PAH Sorption to Nanoplastics and the Trojan Horse Effect as Drivers of Mitochondrial Toxicity and PAH Localization in Zebrafish

Trevisan

Uzochukwu

Giulio

2020

Front. Environ. Sci.

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“…Increasing evidence is becoming available on defects of swim bladder inflation in medaka (Oryzias latipes), a species with only one swim bladder chamber Dong et al, 2016;Mu et al, 2017;Pandelides et al, 2021). Exposure to T3, methimazole, heptafluorobutanoic acid (PFBA) and tris[1,3-dichloro-2-propyl] phosphate (TDCPP) inhibited inflation of the swim bladder in female medaka.…”

Section: Domain Of Applicabilitymentioning

confidence: 99%

Deiodinase 2 inhibition leading to increased mortality via reduced posterior swim bladder inflation

2022

OECD Series on Adverse Outcome Pathways

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This AOP describes the sequence of events leading from deiodinase inhibition to increased mortality via reduced posterior swim bladder inflation. Disruption of the thyroid hormone system is increasingly being recognized as an important toxicity pathway that can cause many adverse outcomes, including developmental abnormalities. Three types of iodothyronine deiodinases (DIO1-3) have been described in vertebrates that activate or inactivate THs and are therefore important mediators of thyroid hormone (TH) action. Type II deiodinase (DIO2) has thyroxine (T4) as a preferred substrate and is mostly important for converting T4 to the more biologically active triiodothyronine (T3). Inhibition of DIO2 therefore reduces T3 levels. As in amphibians, the transition between the different developmental phases in fish, including maturation and inflation of the swim bladder, is mediated by THs (Brown et al., 1988;. The swim bladder is a gas-filled organ that typically consists of two chambers (Robertson et al., 2007). The posterior chamber inflates during early development in the embryonic phase, while the anterior chamber inflates during late development in the larval phase. This AOP describes how DIO2 inhibition results in reduced T3 levels, which prohibit normal inflation of the posterior chamber of the swim bladder in the embryonic phase. The posterior chamber is important for regulating buoyancy and thus for swimming performance (Robertson et al., 2007). Reduced swimming performance reduces chances of survival due to a decreased ability to forage and avoid predators. The final adverse outcome is a decrease of the population growth rate. Since many AOPs eventually lead to this more general adverse outcome at the population level, the more specific and informative adverse outcome at the organismal level, increased mortality, is used in the AOP title. Support for this AOP is mainly based on chemical exposures in zebrafish and fathead minnows (

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“…Water hypoxia (O 2 levels: ≤2.8 mg L −1 ; [ 43 ]) is a major limiting environmental factor. It is routinely experienced by aquatic animals, either chronically or on a diel or seasonal basis, and results from complex processes including mixing, air–water exchange, and fluctuations in the pattern of O 2 production and consumption [ 44 , 45 ].…”

Section: The Nos/no System and The Fish Heartmentioning

confidence: 99%

Hypoxic and Thermal Stress: Many Ways Leading to the NOS/NO System in the Fish Heart

et al. 2021

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Teleost fish are often regarded with interest for the remarkable ability of several species to tolerate even dramatic stresses, either internal or external, as in the case of fluctuations in O2 availability and temperature regimes. These events are naturally experienced by many fish species under different time scales, but they are now exacerbated by growing environmental changes. This further challenges the intrinsic ability of animals to cope with stress. The heart is crucial for the stress response, since a proper modulation of the cardiac function allows blood perfusion to the whole organism, particularly to respiratory organs and the brain. In cardiac cells, key signalling pathways are activated for maintaining molecular equilibrium, thus improving stress tolerance. In fish, the nitric oxide synthase (NOS)/nitric oxide (NO) system is fundamental for modulating the basal cardiac performance and is involved in the control of many adaptive responses to stress, including those related to variations in O2 and thermal regimes. In this review, we aim to illustrate, by integrating the classic and novel literature, the current knowledge on the NOS/NO system as a crucial component of the cardiac molecular mechanisms that sustain stress tolerance and adaptation, thus providing some species, such as tolerant cyprinids, with a high resistance to stress.

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Early life co-exposures to a real-world PAH mixture and hypoxia result in later life and next generation consequences in medaka (Oryzias latipes)

Cited by 19 publications

References 108 publications

PAH Sorption to Nanoplastics and the Trojan Horse Effect as Drivers of Mitochondrial Toxicity and PAH Localization in Zebrafish

PAH Sorption to Nanoplastics and the Trojan Horse Effect as Drivers of Mitochondrial Toxicity and PAH Localization in Zebrafish

Deiodinase 2 inhibition leading to increased mortality via reduced posterior swim bladder inflation

Hypoxic and Thermal Stress: Many Ways Leading to the NOS/NO System in the Fish Heart

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