| Target | Nanoparticle | Major outcomes | References | 
      
        | Brain  |   |   |   | 
      
        |   | Silver NP | Time- and dose-dependent increase    in pro-inflammatory cytokine release and correlating increases in    permeability and cytotoxicity of cells. | [65] | 
      
        |   | Silver NP | Dose-dependent accumulation of NP    was observed in the brain and other organs suggesting systemic distribution    after oral administration. ALP and cholesterol increased significantly in    high-dose group (1000 mg/kg/day) indicating hepatotoxicity. | [66] | 
      
        |   | Silver NP | Neurobehavioural abnormalities    were observed in adult zebrafish with increased DA and 5HT turnover in    previously exposed embryos secondary to altered synaptic functioning. | [67] | 
      
        |   | U    (SPION) | Direct inoculation of all 3 SPION    agents resulted in the uptake into the CNS parenchyma. No pathological    changes were detected. | [68] | 
      
        | Liver | Gold NP | Naked NP: severe adverse effects    with resultant death with particles ranging from 8 to 37 nm in diameter.    Microscopically, Kupffer cell activation in the liver and lung parenchymal    destruction was observed. Surface modified NP: elicited increased host immune    response and improved cytocompatibility. | [69] | 
      
        |   | Gold NP | NPs were found to accumulate in    liver and spleen. Significant upregulation of inflammatory cytokines (IL-1,    6, 10 and TNF-α) with subsequent apoptosis of hepatocytes at highest    concentrations (4.26 mg/kg). No significant changes in the liver at    lower doses. | [70] | 
      
        |   | Silver NP | Oxidative stress-mediated    toxicity due to free Ag+liberation.    Induction of pro-apoptotic signals in liver tissues. | [71] | 
      
        |   | Silver NP | NP enter cells which results in    the production of mediators of oxidative-stress. However, protective    mechanisms could be observed which increase GSH production to avoid oxidative    damage. | [72] | 
      
        |   | Silica NP | Significant hepatotoxicity    (degenerative necrosis of hepatocytes) was observed with smaller NP    (<100 nm) whereas no pathological changes were seen with larger    particles (300 or 1000 nm), even at relatively higher concentrations of    NP (100 mg/kg). | [73] | 
      
        | Dermal  | Silver NP  | Reversible hepatotoxicity and    argyria-like discoloration of treated area of skin, elevated plasma and urine    silver concentrations and increased liver enzymes. | [74] | 
      
        |   | Titanium Dioxide NP | Cytotoxicity was observed affecting    cellular functions such as cell proliferation, differentiation and mobility    resulting in apoptosis. | [75] | 
      
        |   | Silica NP | Size-related toxicity with faster    cellular uptake of smaller particles and concomitant higher toxicity. | [76] | 
      
        |   | Silica NP | Reduced Cell Viability | [77]  | 
      
        |   | Gold NP | Maximum cytotoxicity with smaller    NP (1.4 nm) characterized by apoptosis and necrosis. | [78] | 
      
        |   | Gold NP  | Dose-dependent reduction in cell    proliferation. | [79] | 
      
        | Lung | PLGA-Chitosan NP | Non-toxic even at highest    concentrations. | [80] | 
      
        |   | SWCNP | Low acute cytotoxicity was    further reduced by dispersion of SWCNTs in serum. | [81] | 
      
        |   | MWCNP | Uniform particle uptake by    pulmonary macrophages. No inflammatory or fibrotic changes were observed. | [82] | 
      
        |   | Silica NP | Dose- and time-dependent decrease    in cell viability: up to 50% reduction at highest dosage after 72 h.    Oxidative stress indicated as mechanism of cytotoxicity. | [83] | 
      
        |   | Silica NP | Dose dependent Increase in    Cytotoxicity  | [84]  | 
      
        |   | Silver NP | Dose- and time-dependent increase    in blood Ag nanoparticle concentration was observed along with correlating    increases in alveolar inflammation and small granulomatous lesions. | [85] |