Table 1
Summary of the toxicological studies of n-CeO2 in several aquatic species
| Aquatic species | Characters of n-CeO2 and exposure conditions | Target tissue | Uptake | Toxicological effects | References | ||
|---|---|---|---|---|---|---|---|
| Particle size (nm) | Concentration and exposure method | Exposure | |||||
| 1. Finfish | ↑Plasma cortisol and glucose levels | ||||||
| C.commersonii | 227 | 1.0 mg/L | 25 h | Heart Gills | Gills | ↑ MDA levels. Did not altered RBCs counts. | Rundle et al. (2016) |
| C. auratus | 20 to 40 | 160 up to 320 mg/L | N/A | Brain, gills, and liver | Gills | ↓AChE,SOD and Na+/K+-ATPase activites. ↓ CAT level. | Jun et al. (2013) |
| O. mykiss | <25 | 10 μg/L | 96 h | Gills, liver | Gills | ↑ nCeO2 accumulation ↑ mortality rate | Correia et al. (2019) |
| <50 | 0.1, 0.01, and 0.001 μg/L | 28 d | Gills, brain, liver, eyes | N/A | ↑ GST activity in gills ↑ CAT activity in livers ↓ AChE in fish eyes Induced Histopathological alteration in gills and liver | Bour et al. (2015) | |
| D. rerio | 10.2±0.78 | 500 and 5000 μg/L | 21 d | Gill, liver, skin, brain, gut, blood and kidney | liver | ↑ n-CeO2 accumulation | Felix et al. (2013) |
| D. rerio embryos | 10.2±0.78 | 500 and 5000 μg/L | 7 d | brain, gills, skin and liver | Liver | ↑accumulation in brain, gills and skin | Jemec et al. (2015) |
| 53.3±3.12 | 7.5 x 10–7 mg | 96 h | N/A | N/A | ↓ gross developmental | Jemec et al. (2012) | |
| <25 nm | 0.001, 0.01, 0.1, and 1 mg/L | 96 h | N/A | N/A | ↓Embryo malformations | Khan et al. (2018) | |
| 10–30 | 20, 50, and 100 mg/L | 5 dpf | Digestive system | N/A | ↑ 5-HT level | Özel et al. (2013) | |
| 10–15 | 1, 10, 50 and 100 mg/L | 4 dpf | N/A | N/A | ↓ larvae growth | Felix et al. (2013) | |
| 2. Crustacea | |||||||
| D. magna neonates | 6.5 | 0.011− 0.015 mg/ml | 48 h | N/A | N/A | LC50 = 0.012 mg/mL | Gaiser et al. (2012) |
| D. similis D. pulex | 3±1 | 1, 10 and 100 mg/L | 48 h | N/A | N/A | D. similis 350 times more sensitive ↓ Swimming velocities to 30% and 40% at 1 mg/L in D. pulex and D. similis | Jemec et al. (2012) |
| D. magna neonates | <25 | 0-10 μg/ml | 96 h | N/A | N/A | ↓ tissue accumuation No significant mortalities | Auffan et al. (2013) |
| <25 | 0 to 10 mg/L 0, 0.1, 1, 3 & 10 mg/L | 96 h 21 d | N/A | N/A | 100% mortality at 10 mg/L (after 7 d) 30% mortality at 3 mg/L (over 21 d) | ||
| 3. Bivalves | 24±3 | 1 mg/l to 10 mg/L | 24, 48, 72, and 96 h | soft tissues | Pseudo feces | ↑accumulation (62 μg/g) | García et al. (2011) |
| 15-30 | 1, 5, 10 µg/mL | from 30 min to 4 h | Hemocytes | N/A | ↓ Total extracellular oxyradical production Induced mitochondrial damage, cardiolipin oxidation | Lee et al. (2009) | |
| M. galloprovincialis | 67±8 × 8±31 | 1, 2, or 3 mg/L | 35 days | Soft tissues | Pseudo feces | Not affect Ce accumulation in mussel tissue ↑ Clearance rate | Auguste et al. (2019) |
| 26 ± 16. 9 ± 4 | 1, 10 and 50 mg/L | from 30 min to 4 h | Hemocytes | blood | Negative impacts on hemocytes | Montes et al. (2012) | |
| 20–25 | 100 μg/L | 96 h | Gills, digestive gland Hemocytes | blood | ↑ ROS production and serum LYZ activity ↑ CAT in gills and digestive gland ↑ GST in digesive gland ↓ lysosomal lipofuscin accumulation ↑ Embryotoxicity | Sendra et al. (2018) | |
| D.polymorpha | 3−4 | (Citrate-coated n-CeO2)1 mg/L | 21 d | Digestive gland | Digestive gland | ↑ Removal of n-CeO2 from the water ↓ Bioaccumulation in mussels | Garaud et al. (2016) |
| C. fluminea | 20–25 | 10 and 100 μg/L | 6 days | Digestive gland | Digestive gland | ↑ DNA damage ↑ T-AOC, CAT, GST, caspase-3 No differences in Ce bioaccumulation | Koehlé-Divo et al. (2018) |
Abbreviations: T-AOC: Total antioxidant capacity, CAT: Catalase, GST: Glutathione-S-transferase, LYZ: Lysozyme, ROS: Reactive oxygen species, AChE: Acetyl choline esterase, SOD: Superoxide dismutase, RBCs: Red blood cells, MDA: Malondialdehyde, Ce: cerium.
↑ = means increase and ↓ = means decrease while N/A = means not indicated in the current investigation.
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