Aims: To value the antioxidant effect of vitamin C on atherogenesis induced by oxidative stress, using nitric oxide, superoxide dismutase and nitrotyrosine as biomarkers.Main methods: Wistar rats were used: (A) Control; (B) Proinflammatory Induction for 30 days, (C) Proinflammatory Induction for 30 days+Vitamin C, (D) Proinflammatory Induction for 60 days and (E) Proinflammatory Induction for 60 days+Vitamin C. Proinflammatory Induction with adrenaline (0.1 mg/day/rat). Vitamin C (2,14 mg/day/rat) administered 20 days in (C) and 50 days in (E). Nitric oxide (NO) (µM) and superoxide dismutase(U/ml) were estimated employing spectrophotometry, nitrotyrosine (nM) employing Elisa and histopathological sections were analyzed by optical microscopy. ANOVA was used for quantitative variables and square Chi was used for categorical variables, significance p<0.05 was stablished in all cases. Key findings: In groups (B) (12.23±1.14) and (D) (17.84±1.7) NO decreased compared with (A) (22.46±1.24) (p<0.001, p<0.01). NO normalization was found in (E) (21.78±1.9). Superoxide dismutase showed significantly increased in (B) (159.33±5.56) and (D) (241±5.6) compared to (A) (128.7±5) (p<0.01, p<0.001). Similar augment showed groups (C) (185.12±6.3) and (E) (298.75±3.17) compared with (A) (p<0.01, p<0.001). Nitrotyrosine was increased in (B) (5.03±0.1) and (D)(5.31±0.12) according to proinflammatory induction and decreased in (C) (2.28±0.32) when compared with (B) (p<0.001). Similar response showed (E) (0.73±0.4) compared with (D) (p<0.001). In groups (B) and (D) showed endothelial denudation, intimal thickening and vascular layers disorganization. Group (E) showed a reversal of the lesions described.Significance: nitrotyrosine is a useful marker of peroxynitrite production and oxidative damage to endothelial cells. Vitamin C reversed the oxidative stress but did not reverse the atherogenic lesions in endothelial.