AIM:To evaluate the potential of S-nitroso-N-acetyl-cysteine(SNAC)in inhibition of lipid peroxidation andthe effect of oral SNAC administration in the preventionof nonalcoholic fatty liver disease(NAFLD)in an animalmodel.METHODS:NAFLD was induced in Wistar male rats bycholine-deficient diet for 4 wk.SNAC-treated animals(n=6)(1.4 mg/kg/day of SNAC,orally)were comparedto 2 control groups:one(n=6)received PBS solutionand the other(n=6)received NAC solution(7 mg/kg/d).Histological variables were semiquantitated with respectto macro and microvacuolar fat changes,its zonal dis-tribution,foci of necrosis,portal and perivenular fibro-sis,and inflammatory infiltrate with zonal distribution.LOOHs from samples of liver homogenates were quanti-fied by HPLC.Nitrate levels in plasma of portal vein wereassessed by chemiluminescence.Aqueous low-densitylipoprotein(LDL)suspensions(200 μg protein/mL)wereincubated with CuCl_2(300 μmol/L)in the absence andpresence of SNAC(300 μmol/L)for 15 h at 37℃.Extentof LDL oxidation was assessed by fluorimetry.Linoleicacid(LA)(18.8 μmol/L)oxidation was induced by soy-bean lipoxygenase(SLO)(0.056 μmol/L)at 37℃ in the presence and absence of N-acetylcysteine(NAC)andSNAC(56 and 560 μmol/L)and monitored at 234 nm.RESULTS:Animals in the control group developed mod-erate macro and microvesicular fatty changes in peripor-tal area.SNAC-treated animals displayed only discretehistological alterations with absence of fatty changes anddid not develop liver steatosis.The absence of NAFLD inthe SNAC-treated group was positively correlated with adecrease in the concentration of LOOH in liver homog-enate,compared to the control group(0.7±0.2 nmol/mgvs 3.2±0.4 nmol/mg protein,respectively,P<0.05),whileserum levels of aminotransferases were unaltered.Theability of SNAC in preventing lipid peroxidation was con-firmed in in vitro experiments using LA and LDL as modelsubstrates. AIM: To evaluate the potential of S-nitroso-N-acetyl-cysteine ​​(SNAC) in inhibition of lipid peroxidation and the effect of oral SNAC administration in the prevention of nonalcoholic fatty liver disease (NAFLD) in an animal model. METHODS: NAFLD was induced in Wistar male rats bycholine-deficient diet for 4 wk. SNAC-treated animals (n = 6) (1.4 mg / kg / day of SNAC, orally) were compared to 2 control groups: one (n = 6) received PBS solution and the other n = 6) received NAC solution (7 mg / kg / d). Histological variables were semiquantitated with respectto macro and microvacuolar fat changes, its zonal dis-tribution, foci of necrosis, portal and perivenular fibro-sis, and inflammatory infiltrate with zonal distribution.LOOHs from samples of liver homogenates were quanti-fied by HPLC. Nitrate levels in plasma of portal vein were assessed by chemiluminescence. Aqueous low-density lipoprotein (LDL) suspensions were incubated with CuCl 2 (300 μmol / L) in the absence and presence of SNAC (300 μmol / L) for 15 h at 37 ° C.Ex Toxicity of induced by soy-bean lipoxygenase (SLO) (0.056 μmol / L) at 37 ℃ in the presence of absence of N-acetylcysteine ​​(NAC) andSNACs (56 and 560 μmol / L) and monitored at 234 nm.RESULTS: Animals in the control group developed mod-erate macro and microvesicular fatty changes in peripor-tal area. SNAC-treated animals displayed only discretehistological alterations with absence of fatty changes anddid not develop liver steatosis. The absence of NAFLD inthe SNAC-treated group was positively correlated with adecrease in the concentration of LOOH in liver homog-enate, compared to the control group (0.7 ± 0.2 nmol / mg vs 3.2 ± 0.4 nmol / mg protein , respectively, P <0.05), while the levels of aminotransferases were unaltered. The ability of SNAC in preventing lipid peroxidation was con-firmed in vitro experiments using LA and LDL as modelsubstrates.