Long-term atorvastatin treatment decreases heart maximal oxygen consumption and its vulnerability to in vitro oxidative stress in Watanabe heritable hyperlipidemic rabbit
| Autor: | Michael Theron, Jacques Mansourati, Romain Didier, Christine Moisan, M. Yassine Mallem, Jean-Claude Desfontis, Karine Pichavant-Rafini, Florine Tissier, Clothilde Philouze, Firas Farhat, Martine Gilard, Aline Amérand |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Male Antioxidant Time Factors Physiology medicine.medical_treatment Atorvastatin 030204 cardiovascular system & hematology Pharmacology medicine.disease_cause Mitochondria Heart Hyperlipoproteinemia Type II 03 medical and health sciences Basal (phylogenetics) 0302 clinical medicine Oxygen Consumption Physiology (medical) medicine Animals chemistry.chemical_classification Reactive oxygen species business.industry Myocardium Cardiac muscle VO2 max Heart General Medicine Metabolism Disease Models Animal Oxidative Stress 030104 developmental biology medicine.anatomical_structure chemistry Cardiovascular Diseases Rabbits Hydroxymethylglutaryl-CoA Reductase Inhibitors business Reactive Oxygen Species Oxidative stress medicine.drug |
| Zdroj: | Canadian journal of physiology and pharmacology. 96(11) |
| ISSN: | 1205-7541 |
| Popis: | Statins are currently used in prevention of cardiovascular diseases in high-risk populations, and could be considered in primary prevention. However, few studies are available on the long-term effects of low doses of statins, especially on mitochondrial function and reactive oxygen species (ROS) metabolism at cardiac level. This study aimed to determine potential effects of a long-term atorvastatin treatment, at low-dose concentration, on the myocardium mitochondrial respiration. Thirty-four Watanabe rabbits were treated or not with atorvastatin (2.5 mg·kg-1·day-1) from the age of 3 to 12 months. Every 3 months, proton leak, basal (V0), and maximal (Vmax) mitochondrial respiration on cardiac permeabilized fibers were measured. Additionally, the vulnerability to ROS, cardiac enzymatic antioxidant defenses, and oxidative damage (lipoperoxidation) were analyzed. Proton leak increased over the duration of the experiment (up to 60% from Vmax at 12 months). Moreover, the statin treatment induced a decrease of Vmax and a decrease of ROS susceptibility of cardiac mitochondria. However, the lipoperoxidation and the antioxidant defenses were not dependent on the presence of statin treatment, or on its duration. This is the first study showing a protective effect of long-term statins treatment against the ROS susceptibility in the cardiac muscle. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|