Accumulation and toxicity of CuO and ZnO nanoparticles through waterborne and dietary exposure of goldfish (<i>Carassius</i><i>auratus</i>)

Ateş, Mehmet; Arslan, Zikri; Demir, Veysel; Daniels, James; Farah, Ibrahim

doi:10.1002/tox.22002

Cited by 81 publications

(45 citation statements)

References 51 publications

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“…The observation of a recovery in f h after 25 h nZnO exposure in the current study supports this possibility but chronic exposure studies and supporting information on the fate of nZnO over time are needed to confirm this. Ates et al (2014) noted the presence of substantial levels of free Zn 2+ in nZnO exposure water after 21 d, but no dissolution was observed here so it is unlikely that toxicity was associated with free Zn 2+ in the water. However, dissolution of nZnO may have occurred upon interaction with mucus on the surface of the gill.…”

Section: Gill Damage and Osmoregulatory Responses To Nznocontrasting

confidence: 55%

“…In contrast, goldfish (C. auratus) exposed to comparable levels of nZnO for 21 d showed no increase in gill tissue MDA levels, despite evidence of tissue zinc accumulation (Ates et al, 2014). During prolonged exposures, nZnO aggregation may lead to a reduction in bioactivity, allowing animals to recover.…”

Section: Gill Damage and Osmoregulatory Responses To Nznomentioning

confidence: 91%

“…We have previously shown that acute aquatic nZnO exposure (1.0 mg L À1 for 25 h) can trigger oxidative stress responses in the liver of a freshwater fish, white sucker (Catostomus commersonii), including increases in total glutathione, inactivation of aconitase, and inhibition of glucose-6-phosphate dehydrogenase activity (Dieni et al, 2014). Zinc accumulation was also noted in liver, gill, and intestinal tissue of goldfish (Carassius auratus) exposed to a comparable level of nZnO for 21 d (Ates et al, 2014), implying that ENMs (or Zn 2+ released as a result of ENM dissolution), were taken up from the water. Similar accumulation was observed in carp (Cyprinus carpio) exposed to 50 mg L À1 nZnO for 30 d and those animals exhibited a number of indicators of oxidative stress (Hao et al, 2013).…”

Section: Introductionmentioning

confidence: 91%

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Cardiorespiratory toxicity of environmentally relevant zinc oxide nanoparticles in the freshwater fishCatostomus commersonii

Bessemer¹,

Butler²,

Tunnah³

et al. 2014

Nanotoxicology

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The inhalation of zinc oxide engineered nanomaterials (ENMs) has been linked to cardiorespiratory dysfunction in mammalian models but the effects of aquatic ENM exposure on fish have not been fully investigated. Nano-zinc oxide (nZnO) is widely used in consumer products such as sunscreens and can make its way into aquatic ecosystems from domestic and commercial wastewater. This study examined the impact of an environmentally relevant nZnO formulation on cardiorespiratory function and energy metabolism in the white sucker (Catostomus commersonii), a freshwater teleost fish. Evidence of oxidative and cellular stress was present in gill tissue, including increases in malondialdehyde levels, heat shock protein (HSP) expression, and caspase 3/7 activity. Gill Na(+)/K(+)-ATPase activity was also higher by approximately three-fold in nZnO-treated fish, likely in response to increased epithelial permeability or structural remodeling. Despite evidence of toxicity in gill, plasma cortisol and lactate levels did not change in animals exposed to 1.0 mg L(-1) nZnO. White suckers also exhibited a 35% decrease in heart rate during nZnO exposure, with no significant changes in resting oxygen consumption or tissue energy stores. Our results suggest that tissue damage or cellular stress resulting from nZnO exposure activates gill neuroepithelial cells, triggering a whole-animal hypoxic response. An increase in parasympathetic nervous signaling will decrease heart rate and may reduce energy demand, even in the face of an environmental toxicant. We have shown that acute exposure to nZnO is toxic to white suckers and that ENMs have the potential to negatively impact cardiorespiratory function in adult fish.

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Section: Gill Damage and Osmoregulatory Responses To Nznocontrasting

confidence: 55%

Section: Gill Damage and Osmoregulatory Responses To Nznomentioning

confidence: 91%

Section: Introductionmentioning

confidence: 91%

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Cardiorespiratory toxicity of environmentally relevant zinc oxide nanoparticles in the freshwater fishCatostomus commersonii

Bessemer¹,

Butler²,

Tunnah³

et al. 2014

Nanotoxicology

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“…Gills, liver, kidney, intestine, brain, spleen and muscle tissue were collected and washed with ultrapure water. The samples were prepared for instrumental analysis according to methods described previously (Arslan et al, 2011; Ates et al, 2015). About 0.2 to 0.5 g samples (wet weight) were dried in an incubator for 2 days at 100 °C.…”

Section: Methodsmentioning

confidence: 99%

Chronic exposure of tilapia (Oreochromis niloticus) to iron oxide nanoparticles: Effects of particle morphology on accumulation, elimination, hematology and immune responses

et al. 2016

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Effects of chronic exposure to alpha and gamma iron oxide nanoparticles (α-Fe2O3 and γ-Fe2O3 NPs) were investigated through exposure of tilapia (Oreochromis niloticus) to 0.1, 0.5 and 1.0 mg/L (9.2×10−4, 4.6×10−3 and 9.2×10−3 mM) aqueous suspensions for 60 days. Fish were then transferred to NP-free freshwater and allowed to eliminate ingested NPs for 30 days. The organs, including gills, liver, kidney, intestine, brain, spleen, and muscle tissue of the fish were analyzed to determine the accumulation, physiological distribution and elimination of the Fe2O3 NPs. Largest accumulation occurred in spleen followed by intestine, kidney, liver, gills, brain and muscle tissue. Fish exposed to γ-Fe2O3 NPs possessed significantly higher Fe in all organs. Accumulation in spleen was fast and independent of NP concentration reaching to maximum levels by the end of the first sampling period (30th day). Dissolved Fe levels in water were very negligible ranging at 4–6 μg/L for α-Fe2O3 and 17–21 μg/L for γ-Fe2O3 NPs (for 1 mg/L suspensions). Despite that, Fe levels in gills and brain reflect more dissolved Fe accumulation from metastable γ-Fe2O3 polymorph. Ingested NPs cleared from the organs completely within 30-day elimination period, except the liver and spleen. Liver contained about 31% of α- and 46% of γ-Fe2O3, while spleen retained about 62% of α- and 35% of the γ-polymorph. No significant disturbances were observed in hematological parameters, including hemoglobin, hematocrit, red blood cell and white blood cell counts (p > 0.05). Serum glucose (GLU) levels decreased in treatments exposed to 1.0 mg/L of γ-Fe2O3 NPs at day 30 (p < 0.05). In contrast, GLU levels increased during the elimination period for 1.0 mg/L α-Fe2O3 NPs treatments (p < 0.05). Transient increases occurred in glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), and lactate dehydrogenase (LDH). Serum Fe levels did not change during exposure (p > 0.05), but increased significantly within elimination period due to mobilization of ingested NPs from liver and spleen to blood. Though respiratory burst activity was not affected (p > 0.05), lysozyme activity (LA) was suppressed suggesting an immunosuppressive effects from both Fe2O3 NPs (p < 0.05). In contrast, myeloperoxidase (MPO) levels increased significantly in treatments exposed to α-Fe2O3 NPs (p < 0.05), and the effect from γ-polymorph was marginal (p ≥ 0.05). The results indicate that morphological differences of Fe2O3 NPs could induce differential uptake, assimilation and immunotoxic effects on O. niloticus under chronic exposure.

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“…Wet artemia samples from short-term and long-term exposures were digested in HNO 3 according to protocols described elsewhere (Arslan et al 2011; Ates et al 2015b) and were analyzed by ICP-MS. Data collection was performed by ICP–MS Expert software package (version 2.2 b126) using 60 Ni and 59 Co isotopes of Ni and Co. Germanium ( 72 Ge) was used as an internal standard (IS) element. The IS solution (5.0 μg L −1 Ge in 1% HNO 3 ) was mixed online with the sample solution.…”

Section: Methodsmentioning

confidence: 99%

Toxicity of Engineered Nickel Oxide and Cobalt Oxide Nanoparticles to Artemia salina in Seawater

Ateş

Demir

Arslan

et al. 2016

Water Air Soil Pollut

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In this study, the effects of exposure to engineered nickel oxide (NiO 40–60 nm) and cobalt oxide (CoO <100 nm) nanoparticles (NP) were investigated on Artemia salina. Aggregation and stability of the aqueous NP suspensions were characterized by DLS and TEM. Acute exposure was conducted on nauplii (larvae) in seawater in a concentration range from 0.2 to 50 mg/L NPs for 24 h (short term) and 96 h (long term). The hydrodynamic diameters of NiO and CoO NPs in exposure medium were larger than those estimated by TEM. Accumulation rate of NiO NPs were found to be four times higher than that of CoO NPs under the same experimental conditions. Examinations under phase contrast microscope showed that the nanoparticles accumulated in the intestine of artemia, which increased with increasing exposure concentration. Differences were observed in the extent of dissolution of the NPs in the seawater. The CoO NPs dissolved significantly while NiO NPs were relatively more stable. Oxidative stress induced by the NP suspensions was measured by malondialdehyde assay. Suspensions of NiO NPs caused higher oxidative stress on nauplii than those of CoO NPs. The results imply that CoO and NiO NPs exhibit toxicity on artemia (e.g., zooplankton) that are an important source of food in aquatic food chain.

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Accumulation and toxicity of CuO and ZnO nanoparticles through waterborne and dietary exposure of goldfish (Carassiusauratus)

Cited by 81 publications

References 51 publications

Cardiorespiratory toxicity of environmentally relevant zinc oxide nanoparticles in the freshwater fishCatostomus commersonii

Cardiorespiratory toxicity of environmentally relevant zinc oxide nanoparticles in the freshwater fishCatostomus commersonii

Chronic exposure of tilapia (Oreochromis niloticus) to iron oxide nanoparticles: Effects of particle morphology on accumulation, elimination, hematology and immune responses

Toxicity of Engineered Nickel Oxide and Cobalt Oxide Nanoparticles to Artemia salina in Seawater

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