Table 2 NM-induced injuries that contribute to NASH

ZnO-NPs

30 nm

Hens (Jinghong1 strain)

10 mg/kg b.w., oral administration, 4 and 24 w

Caused plasma metabolomic perturbations correlated with hepatic steatosis

[7]

Cu-NPs

23.5 nm

ICR mice

341–1080 mg/kg b.w., oral administration, 48 h

Induced hepatic steatosis

[37]

Au-NPs

20 nm

Wistar rats

0.01 mg/kg b.w., intravenous injection, 2 months

Induced alterations in gene expression related to lipid metabolism in the liver

[38]

CeO₂-NPs

8 nm

HepG2 cells

6.25–200 μg/mL, 24 h

Induced oxidative stress and increased the content of many lipids, particularly FFAs

[40]

CeO₂-_, SiO₂-_, TiO₂-_, CuO-NPs

5 to > 500 nm

HepG2 cells

3 μg/mL for CuO, 30 μg/mL for CeO₂ and SiO₂, and 100 μg/mL for CeO₂; 72 h

Triggered oxidative stress and increased lipid concentrations

[39]

Au nanospheres and nanostars

40 nm

Wistar rats

1.33 × 10¹¹/kg b.w., intravenous administration, 24 h

Triggered oxidative stress and increased FFA levels

[41]

MWCNTs

Diameter: 12.5 ± 2.5 nm, length: 13.0 ± 1.5 mm

C57BL/6 J mice

0.1 mg/mice, intratracheal administration, 1 year

Induced inflammation, steatosis, and fibrosis in the liver

[56]