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Iranian Journal of Pharmaceutical Sciences
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Nasoohi, S., Naserzadeh, P., Rahmanabadi, N., Saiid, B., Pourahmad Jaktaji, J. (2017). Toxicity of atorvastatin on isolated brain mitochondria. Iranian Journal of Pharmaceutical Sciences, 13(2), 1-12. doi: 10.22034/ijps.2017.31107
Sanaz Nasoohi; Parvaneh Naserzadeh; Nafiseh Rahmanabadi; Banafsheh Saiid; Jalal Pourahmad Jaktaji. "Toxicity of atorvastatin on isolated brain mitochondria". Iranian Journal of Pharmaceutical Sciences, 13, 2, 2017, 1-12. doi: 10.22034/ijps.2017.31107
Nasoohi, S., Naserzadeh, P., Rahmanabadi, N., Saiid, B., Pourahmad Jaktaji, J. (2017). 'Toxicity of atorvastatin on isolated brain mitochondria', Iranian Journal of Pharmaceutical Sciences, 13(2), pp. 1-12. doi: 10.22034/ijps.2017.31107
Nasoohi, S., Naserzadeh, P., Rahmanabadi, N., Saiid, B., Pourahmad Jaktaji, J. Toxicity of atorvastatin on isolated brain mitochondria. Iranian Journal of Pharmaceutical Sciences, 2017; 13(2): 1-12. doi: 10.22034/ijps.2017.31107

Toxicity of atorvastatin on isolated brain mitochondria

Article 1, Volume 13, Issue 2, Spring 2017, Page 1-12  XML PDF (674.1 K)
Document Type: Research Paper
DOI: 10.22034/ijps.2017.31107
Authors
Sanaz Nasoohi1; Parvaneh Naserzadeh2; Nafiseh Rahmanabadi2; Banafsheh Saiid2; Jalal Pourahmad Jaktaji email 1
1a Department of Pharmacology and Toxicology, Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, P.O. Box 14155-6153, Tehran, Iran. bPharmaceutical Sciences Research Center, Shahid Beheshti University of Medical Sciences, P.O. Box 14155-6153, Tehran, Iran.
2a Department of Pharmacology and Toxicology, Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, P.O. Box 14155-6153, Tehran, Iran. bPharmaceutical Sciences Research Center, Shahid Beheshti University of Medical Sciences, P.O. Box 14155-6153, Tehran, Iran. cStudents Research Committee, School of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran
Abstract
Background: Although the bio kinetics, metabolism and chemical toxicity of Atorvastatin are well known, until recently little attention was paid to the potential neurotoxic effect of Atorvastatin (Atv). Regarding the concrete evidences indicating Atv may reduce Coenzyme Q10 (CoQ10) levels through blockage of  metalonate cycle, the present work aims to determine if Atorvastatin may provide toxic effects on brain mitochondria and whether its supplementation with two lipidicantioxidants, CoQ10 and Vit E may improve such outcomes.
Methods: to evaluate mitochondrial toxicity, male NMRI mice were first treated with Atorvastatin(bo; 20 and 60 mg/kg) every other day with or without supplementation with CoQ10 (200 mg/kg) or Vit E (40 u/kg). After a period of 4 weeks, the animals were euthanized and brain cortices were harvested ad subjected to mitochondria isolation procedure. ROS release, mitochondrial membrane potential (MMP) and cytochrome c release were performed to precisely address the probable mitochondrial injury.
Findings: Our data showed increased ROS formation, MMP collapse, mitochondrial swelling and cytochrome c release in Atorvastatin treated mice, suggesting that mitochondrial ROS formation and apoptosis signaling are likely involved in Atorvastatin neurotoxicity. Importantly according to the data from animals receiving either CoQ10 or Vit E, supplementation with these lipophilic antioxidants, remarkable reverted the corresponding Atorvastatin mitochondrial toxicity markers.
Concusion: Conclusively the present work addresses chronic Atorvastatin toxic effects on brain mitochondria and supports advantages of Vit E or CoQ10 supplementation. Whether such neurotoxic effect is correlated with CoQ10 depletion or if the improving effects of the due supplementation contribute toAtorvastatin receiving patients, needs more investigations.
Keywords
Atorvastatin; Mitochondria; Apoptosis; brain; E vitamin; CoQ10
Main Subjects
Pharmacology and toxicology
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