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Advances in Medicine
Volume 2014 (2014), Article ID 947258, 6 pages
Research Article

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

1Cátedra de Física Biomédica, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, X5000 Córdoba, Argentina
2Instituto de Investigación en Ciencias de la Salud Humana (IICSHUM), Universidad Nacional de La Rioja, La Rioja, Argentina
3Becaria Secyt, Universidad Nacional de Córdoba, Córdoba, Argentina
4Cátedra de Física Biomédica, Facultad de Ciencias Médicas, Universidad Nacional de La Rioja, F5300 La Rioja, Argentina

Received 23 July 2014; Revised 29 September 2014; Accepted 29 September 2014; Published 23 October 2014

Academic Editor: João Quevedo

Copyright © 2014 María de la Paz Scribano et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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; 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 (), but it decreased after administration of atorvastatin in AI-Ator (). NO diminished in AI relative to Ctr and increased in AI-Ator (). SOD showed an increase in AI and AI-Ator compared to Ctr (). 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.