Brine shrimp (Artemia salina) larvae were exposed to different sizes of zinc (Zn) and zinc oxide (ZnO) nanoparticles (NPs) to evaluate their toxicity in marine aquatic ecosystems. Acute exposure was conducted in seawater with 10, 50 and 100 mg L⁻¹ concentrations of the NPs for 24 h and 96 h. Phase contrast microscope images confirmed the accumulation of the NPs inside the guts. Artemia were unable to eliminate the ingested particles, which was thought to be due to the formation of massive particles in the guts. Although the suspensions of the NPs did not exhibit any significant acute toxicity within 24 h, mortalities increased remarkably in 96 h and escalated with increasing concentration of NP suspension to 42% for Zn NPs (40–60 nm) (LC₅₀ ∼ 100 mg L⁻¹) and to about 34% for ZnO NPs (10–30 nm) (LC₅₀ > 100 mg L⁻¹). The suspensions of Zn NPs were more toxic to Artemia than those of ZnO NPs under comparable regimes. This effect was attributed to higher Zn²⁺ levels (ca. up to 8.9 mg L⁻¹) released to the medium from Zn NPs in comparison to that measured in the suspensions of ZnO NPs (ca. 5.5 mg L⁻¹). In addition, the size of the nanopowders appeared to contribute to the observed toxicities. Although the suspensions possessed aggregates of comparable sizes, smaller Zn NPs (40–60 nm) were relatively more toxic than larger Zn NPs (80–100 nm). Likewise, the suspensions of 10–30 nm ZnO NPs caused higher toxicity than those of 200 nm ZnO NPs. Lipid peroxidation levels were substantially higher in 96 h (p < 0.05), indicating that the toxic effects were due to the oxidative stress.

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 1.0mg/L (9.2×10(-4), 4.6×10(-3) and 9.2×10(-3)mM) aqueous suspensions for 60days. Fish were then transferred to NP-free freshwater and allowed to eliminate ingested NPs for 30days. 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 4-6μg/L for α-Fe2O3 and 17-21μg/L for γ-Fe2O3 NPs (for 1mg/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 1.0mg/L of γ-Fe2O3 NPs at day 30 (p<0.05). In contrast, GLU levels increased during the elimination period for 1.0mg/L α-Fe2O3 NPs treatments (p0.05), 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.