Relationship between hyperfibrinogenemia (HF), oxidative stress, and atherogenesis was established. Effect of atorvastatin (Ator) was assessed. Wistar male (6 months) rats were studied: Ctr, control, without HF induction; Ctr-Ator, without HF treated with atorvastatin; AI, atherogenesis induced, and AI-Ator, atherogenesis induced and treated with atorvastatin. Atherogenesis was induced by daily adrenaline injection (0.1 mL/day/rat) for 90 days; treatment started 15 days after induction. Fibrinogen (mg/dL) and nitric oxide (NO) were measured in plasma (mM) and superoxide dismutase (SOD) (U/mL) in red cell lysate by spectrophotometry. Slices of aorta were analyzed by electron microscopy (EM). ANOVA and chi-square test were used; P < 0.05 was established. There were no significant differences between Ctr and Ctr-Atorv in fibrinogen, NO, and SOD values. Comparing Ctr with AI an increase of fibrinogen is observed (P < 0.001), but it decreased after administration of atorvastatin in AI-Ator (P < 0.001). NO diminished in AI relative to Ctr and increased in AI-Ator (P < 0.001). SOD showed an increase in AI and AI-Ator compared to Ctr (P < 0.001). EM revealed expansion of intermembrane space and disorganization of crests in AI. In AI-Ator mitochondrial areas and diameters were similar to control. Atorvastatin normalizes HF, stabilizes NO, increases SOD, and produces a partial regression of mitochondrial lesions.
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.
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