Table 1 : Some of the adverse responses of nanomaterials.

Nanomaterials and parameters Tissues/cells and Responses References

CNT (single walled C-nanotube; 24 mg/ml Plasma membrane destabilized, declined viability, oxidative stress induced
and caused change in ultra structural morphological  changes
Single walled C-nanotubes 200µg/ml Inhibited cell proliferation, induced apoptosis, reduced the ability of cell adhesion, viability loss of embryonic renal cells [81]
Single walled C-nanotubes and multiwalled nanotubes, 22.6µg/ml, 226µg/ml High toxicity in macrophages in alveolar tissue, loss of viability, detachment
of cells and change in protein expression
Single walled nanotubes 24 hr Morphological changes in lamellar structures, microvilli, tonofilaments and desmosome junctions in relation to cell membrane [83]
Al2O3, CeO2, TiO2 metal oxides nanoparticles Change in membrane potential, induce lipid peroxidation and oxidative stress, cytotoxicity was observed,  [84]
Cationic nanoscale materials (related to surface charge) Spherical NPs were taken up 500% more readily than rod shaped NPs, internalized NPs bombarded the endosomes and reached cytosol machinery, cationic  NPs move across the cell membrane by forming transient opening and  due to hydrophobicity, induced cytotoxicity [85]
Silica NPs Resulted cytotoxicity, caused oxidative stress in vivo and in vitro, elevated lipid peroxidation resulting rise in ROS and decline in cellular glutathione (GHS) [58,86]
Gold NPs (AuNPs),  Silver NPs (AgNPs), CoCrNPs Depolarization of α-tubulin, disturbing the cellular structure, partial fragmentation of Protein [60]
Silver zeolite NMs Produces reactive oxygen species [19]
Carbon nanotubes  Causes inflammation in neural cells (glial cells), cytokine [87]
Dextran coated SPION(20nmand 60 nm) Induced proinflammatory cytokine [86]
Colloidal gold NPs (1µM/5µL) Affected electrical activity in retina but no morphological changes [87]
ZnO NPs (50µg/g, 150µg/g ) Atrophy of embryonic hepatic tissue  (chicken) [41]
ZnO NPs (20µg/ml, 30µg/ml) Hemolysis of human red blood cells [42]
Copper NPs 413mg/K-1 5000mg/K-1 Pathological damage to liver, kidney, spleen [39
CdSeQD with ZnO shell 0.014µg/kg/day Increased gastric toxicity in presence of simulated gastric fluid, induce accumulation in body tissues [88]
Silver NPs 125mg/kg, 60nm Elevated cholesterol and cholestric enzyme [88]
Coated QD (bidentate thiolated hydrocarbonic acids, silica, lipid micelles) Induced the release of proinflammatory cytokines leading to cytotoxicity [79]
Gold, silver and ZnO NPs 10 nm; 25, 50 and 100ppm Caused increase in LDH activity [75]
TiO2(in respiratory tract) Caused oxidative damage to DNA and inflammation genetic instability, [89]
TiO2 (industrial grade) Higher degree of deletion of DNA, pups exhibit dose dependent DNA strand breaks [88]
SiO2, ZnO, Fe2O3, Ag, CeO2, Caused dose dependent DNA damage [69]
SWNT, MWNT (less than 2.5 micron
Particulate Matter)
Damaged mtDNA, increased aortic plaque [90]
C60 Nanoparticle Bind to DNA and RNA  and damages them [71]
Polystyrene particles (110nm to 1000nm Affected the intrinsic activity of enzyme model α-chymotrypsin, [72]
anionic MMPCs (protected nanoclusters) Effectively inhibited the chymotrypsin activity. [91]
silicon nanowires (SiNW-SiO2–functionalized with carboxyl group and  highly reactive hydrogen modified (SiNW-H) Inhibited the enzyme activity of restriction endonuclease and Taq DNA polymerase. [92]
Iron oxide NPs  Increased the levels of alkaline phosphatase, aspartate amino transferase
and alanine amino transferase enzyme activities
Iron oxide NPs, 30-35 nm diameter, 7.5,15, 30mg/kg Enzyme activity of GSH, SOD and CAT declined  as the concentration of NPs increased [94]

Lahir Yogendra Kumar Journal of Toxicology and Health  2015 2:2DOI : 10.7243/2056-3779-2-2