Oral administration of S-nitroso-N-acetylcysteine prevents the onset of non alcoholic fatty liver disease in rats

Figure 1 Histological features of liver tissue of rats fed with choline-deficient diet. A: Control group showing a moderate macro and microvacuolar steatosis in periportal zone; B: SNAC-treated animals showing normal liver in periportal zone (hematoxylin-eosin stain-HE); C: Control group showing positive Scharlach staining; D: SNAC-treated animals showing negative Scharlach staining.

Figure 2 Concentration of hydroperoxides (LOOH) in liver homogenates of the control group, NAC and SNAC-treated animals.

Figure 3 Emission spectra of human LDL (200 μg/mL) suspended in aerated PBS. A: Freshly prepared suspension; B: after incubation with CuCl₂ (300 μmol/L) for 15 h; C: after co-incubation with CuCl₂ (300 μmol/L) and SNAC (300 μmol/L). The excitation and emission wavelengths were 360 and 433 nm, respectively.

Figure 4 Kinetic curves of linoleic acid (18. 76 μmol/L) peroxidation catalyzed by SLO (A) (0.056 μmol/L), SLO co-incubated with NAC (B) (560 μmol/L), SLO co-incubated with SNAC (C) (56 μmol/L) and SLO co-incubated with SNAC (D) (560 μmol/L). Absorbance changes were monitored at 234 nm at 37 °C.

Figure 5 Barr graph showing the extent (Ext) and initial rates (V₀) of the peroxidation reaction of linoleic acid (LA) by SLO. Data were extracted from the curves of Figure 4.