Effects of Atorvastatin on Oxidative Stress Biomarkers and Mitochondrial Morphofunctionality in Hyperfibrinogenemia-Induced Atherogenesis

Abstract EN

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.