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. 1. Introduction There is great interest in the prevention of atherogenic disease with a focus on the effectiveness of pharmacological agents, among them, the antioxidants for primary prevention [1, 2]. The evolution of physiopathological knowledge of atherogenesis has given the inflammatory process and oxidative component an importance equivalent to the lipid accumulation in the vascular wall [3, 4]. Cardiovascular risk factors such as hyperfibrinogenemia generate oxidative stress; their toxic effects on biomolecules at the level of vascular layers, associated with the metabolic degradation and redox-sensitive signaling, induce the development of the pathology [5]. The dysfunctional endothelium loses its ability to regulate its vital functions, acquiring procoagulant properties instead of anticoagulant, and reduces the bioavailability of nitric oxide (NO) by oxidative inactivation due to the excessive production of superoxide and hydrogen peroxide in the vascular wall. These changes constitute the most characteristic and the earliest systemic phenomena of the endothelial dysfunction, sine qua non condition for atherogenesis [6, 7]. As we have demonstrated in previous works [8, 9], the endothelial activation induced by
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