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

Scribano Mde L, Baez Mdel C, Florencia B, Tarán MD, Franco S, Balceda AG, Moya M - Adv Med (2014)

Bottom Line: 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).SOD showed an increase in AI and AI-Ator compared to Ctr (P < 0.001).

View Article: PubMed Central - PubMed

Affiliation: Cátedra de Física Biomédica, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, X5000 Córdoba, Argentina.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus

(a) Microphotograph of mitochondria in Ctr group, structure of membranes, and crests without changes and maintaining normal shape and size (arrow), 27800x; (b) Ctr + Ator group showing no changes in shape and size, 21560x; (c) AI group, showing an expansion of the intermembranous space, disorganization of crests, and turbid tumefaction (arrow), 27800x; (d) microphotograph of thoracic aorta of AI-Atorv group, showing mitochondria with unharmed membranes and normal mitochondrial crests, 21560x.
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fig4: (a) Microphotograph of mitochondria in Ctr group, structure of membranes, and crests without changes and maintaining normal shape and size (arrow), 27800x; (b) Ctr + Ator group showing no changes in shape and size, 21560x; (c) AI group, showing an expansion of the intermembranous space, disorganization of crests, and turbid tumefaction (arrow), 27800x; (d) microphotograph of thoracic aorta of AI-Atorv group, showing mitochondria with unharmed membranes and normal mitochondrial crests, 21560x.

Mentions: When the results of the groups with persistent hyperfibrinogenemia and decreased NO were analyzed, the total and mean number of mitochondria decreased significantly in the AI group (Figure 4) in comparison to the Ctr group (Figure 4) (P < 0.001). In addition, there was a marked expansion of the intermembrane space and clearance of the mitochondrial matrix, with disorganized crests and vacuoles and even an apparent absence of crests in some organelles. These changes are compatible with mitochondrial tumefaction. Furthermore, mitochondria presented perinuclear localization associated with several vesicles. Mitochondria in the AI-Ator group treated for 75 days (C) (Figure 4) revealed unharmed membranes and normal mitochondrial crests. Degree of alteration decreased from 3 to 18.75%, which was statistically significant in relation to untreated animals with induced HF (Table 1).


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

Scribano Mde L, Baez Mdel C, Florencia B, Tarán MD, Franco S, Balceda AG, Moya M - Adv Med (2014)

(a) Microphotograph of mitochondria in Ctr group, structure of membranes, and crests without changes and maintaining normal shape and size (arrow), 27800x; (b) Ctr + Ator group showing no changes in shape and size, 21560x; (c) AI group, showing an expansion of the intermembranous space, disorganization of crests, and turbid tumefaction (arrow), 27800x; (d) microphotograph of thoracic aorta of AI-Atorv group, showing mitochondria with unharmed membranes and normal mitochondrial crests, 21560x.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4590975&req=5

fig4: (a) Microphotograph of mitochondria in Ctr group, structure of membranes, and crests without changes and maintaining normal shape and size (arrow), 27800x; (b) Ctr + Ator group showing no changes in shape and size, 21560x; (c) AI group, showing an expansion of the intermembranous space, disorganization of crests, and turbid tumefaction (arrow), 27800x; (d) microphotograph of thoracic aorta of AI-Atorv group, showing mitochondria with unharmed membranes and normal mitochondrial crests, 21560x.
Mentions: When the results of the groups with persistent hyperfibrinogenemia and decreased NO were analyzed, the total and mean number of mitochondria decreased significantly in the AI group (Figure 4) in comparison to the Ctr group (Figure 4) (P < 0.001). In addition, there was a marked expansion of the intermembrane space and clearance of the mitochondrial matrix, with disorganized crests and vacuoles and even an apparent absence of crests in some organelles. These changes are compatible with mitochondrial tumefaction. Furthermore, mitochondria presented perinuclear localization associated with several vesicles. Mitochondria in the AI-Ator group treated for 75 days (C) (Figure 4) revealed unharmed membranes and normal mitochondrial crests. Degree of alteration decreased from 3 to 18.75%, which was statistically significant in relation to untreated animals with induced HF (Table 1).

Bottom Line: 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).SOD showed an increase in AI and AI-Ator compared to Ctr (P < 0.001).

View Article: PubMed Central - PubMed

Affiliation: Cátedra de Física Biomédica, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, X5000 Córdoba, Argentina.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus