Table of Contents
ISRN Cardiology
Volume 2014, Article ID 739526, 6 pages
http://dx.doi.org/10.1155/2014/739526
Research Article

Mitochondrial Morphofunctional Alterations in Smooth Muscle Cells of Aorta in Rats

1Instituto de Investigación en Ciencias de la Salud Humana (IICSHUM), Universidad Nacional de La Rioja, La Rioja, Argentina
2Cátedra de Física Biomédica, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina
3Becaria Secyt, Universidad Nacional de Córdoba, Córdoba, Argentina
4Cátedra de Física Biomédica, Facultad de Ciencias Médicas, Universidad Nacional de La Rioja, La Rioja, Argentina
5Centro de Microscopía Electrónica, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Argentina
6Los Médanos 3155, Alto Verde, 5009 Córdoba, Argentina

Received 20 November 2013; Accepted 19 December 2013; Published 6 February 2014

Academic Editors: P. E. Puddu and A. Stephanou

Copyright © 2014 María del Carmen Baez 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.

Abstract

In an experimental model of atherogenesis induced by hyperfibrinogenemia (HF), the pharmacological response of vitamin E was studied in order to assess its antioxidant effect on the mitochondrial morphofunctional alterations in aortic smooth muscle cells. Three groups of male rats were used: (Ctr) control, (AI) atherogenesis induced for 120 days, and (AIE) atherogenesis induced for 120 days and treated with vitamin E. HF was induced by adrenalin injection (0.1 mg/day/rat) for 120 days. AIE group was treated with the administration of 3.42 mg/day/rat of vitamin E for 105 days after the first induction. Mitochondria morphology was analyzed by electronic microscopy (EM) and mitochondrial complexes (MC) by spectrophotometry. In group AI the total and mean number of mitochondria reduced significantly, the intermembranous matrix increased, and swelling was observed with respect to Ctr and AIE (). These damages were related to a significant decrease in the activity of citrate synthase and complexes I, II, III, and IV in group AI in comparison to Ctr (). Similar behavior was presented by group AI compared to AIE (). These results show that vitamin E produces a significative regression of inflammatory and oxidative stress process and it resolved the morphofunctional mitochondrial alterations in this experimental model of atherogenic disease.