Regular ArticleImmunosuppressive Treatment Affects Cardiac and Skeletal Muscle Mitochondria by the Toxic Effect of Vehicle☆
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Cited by (32)
Cyclosporine A normalizes mitochondrial coupling, reactive oxygen species production, and inflammation and partially restores skeletal muscle maximal oxidative capacity in experimental aortic cross-clamping
2013, Journal of Vascular SurgeryCitation Excerpt :Accordingly, rats fed with CsA 10 mg/kg/d and 25 mg/kg/d for 3 weeks significantly decreased their gastrocnemius V0 (−40% and −45%, respectively), and CsA dose dependently increased the ACR in gastrocnemius muscles.27 Changes in V0 were less marked here, perhaps because of the shorter duration of the experiments, but our results are in line with these data.27 Reduced oxidative stress likely participated in CsA beneficial effects, as other protective approaches such as ischemic postconditioning also decrease IR-induced ROS production and muscle mitochondrial dysfunction.5,8
Kinetic analysis of the toxicity of pharmaceutical excipients cremophor EL and RH40 on endothelial and epithelial cells
2013, Journal of Pharmaceutical SciencesCitation Excerpt :Cremophor EL induced damage in isolated human cancer cells9 and human cell lines including Caco-2.10 These toxic effects are related to inhibition of cardiac mitochondrial respiration,11 cell membrane perturbation,412 and promotion of oxidative stress.8,13 Cremophor RH40 is used in microemulsions,14 in self-emulsifying drug delivery systems,15 in uccoadhesive tablets,16 and in oral formulations, such as Neoral (Novartis, East Hanover, NJ).
Direct, pleiotropic protective effect of cyclosporin A against simulated ischemia-induced injury in isolated cardiomyocytes
2005, European Journal of PharmacologyPreserved response of mitochondrial function to short-term endurance training in skeletal muscle of heart transplant recipients
2003, Journal of the American College of CardiologyCitation Excerpt :The present study shows, for the first time, that skeletal muscle fibers of HTR patients exhibit a normal mitochondrial profile and normal expected responses to physical training, despite immunosuppressive therapy with CsA. Administration of CsA at high dosages decreases mitochondrial respiration in vitro (8,11)and in vivo (9,10)and alters the MyHC and metabolic profile of animal skeletal muscle (28). As we demonstrated that these muscular deleterious effects are due to the vehicle and not to the active molecule (10,11), it is likely that at the clinical doses of oral CsA, the toxic effects of the vehicle on mitochondrial function are not detectable in humans.
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Please address all correspondence to: R. Ventura-Clapier, U-446 INSERM, Cardiologie Cellulaire et Moléculaire, Université Paris-Sud, 92296 Châtenay-Malabry, France. Fax: (+331) 46 83 54 75; E-mail: [email protected]