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Molecular and Biochemical Evidence on the Protection of Cardiomyocytes From Phosphine-Induced Oxidative Stress, Mitochondrial Dysfunction and Apoptosis by Acetyl-L-Carnitine Publisher Pubmed



Baghaei A1, 2 ; Solgi R4, 5 ; Jafari A6 ; Abdolghaffari AH7 ; Golaghaei A1 ; Asghari MH1 ; Baeeri M1 ; Ostad SN1 ; Sharifzadeh M1 ; Abdollahi M2
Authors
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Authors Affiliations
  1. 1. Department of Toxicology and Pharmacology, Faculty of Pharmacy, Alborz University of Medical Sciences, Karaj, Iran
  2. 2. Department of Toxicology and Pharmacology, Faculty of Pharmacy, Pharmaceutical Sciences Research Center
  3. 3. and Poisoning and Toxicology Research Center, Endocrinology and Metabolism Research Center, Endocrinology and Metabolism Clinical Sciences Inst., Tehran, 1417614411, Iran
  4. 4. Metabolic Disorders Research Center, Golestan University of Medical Sciences, Gorgan, Iran
  5. 5. Department of Pharmacology, Faculty of Medicine, Golestan University of Medical Sciences, Gorgan, Iran
  6. 6. Department of Pharmacology and Toxicology, Faculty of Pharmacy, Urmia University of Medical Sciences, Urmia, Iran
  7. 7. Medicinal Plants Research Center, Institute of Medicinal Plants, ACECR, Karaj, Iran

Source: Environmental Toxicology and Pharmacology Published:2016


Abstract

The aim of the present study was to investigate the efficacy of acetyl-l-carnitine (ALCAR) on pathologic changes of mitochondrial respiratory chain activity, ATP production, oxidative stress, and cellular apoptosis/necrosis induced by aluminum phosphide (AlP) poisoning. The study groups included: the Sham that received almond oil only; the AlP that received oral LD50 dose of aluminum; the AC-100, AC-200, and AC-300 which received concurrent oral LD50 dose of AlP and single 100, 200, and 300mg/kg of ALCAR by intraperitoneal injection. After 24h, the rats were sacrificed; the heart and blood sample were taken for measurement of biochemical and mitochondrial factors. The results specified that ALCAR significantly attenuated the oxidative stress (elevated ROS and plasma iron levels) caused by AlP poisoning. ALCAR also increased the activity of cytochrome oxidase, which in turn amplified ATP production. Furthermore, flow cytometric assays and caspase activity indicated that ALCAR prohibited AlP-induced apoptosis in cardiomyocytes. © 2015 Elsevier B.V..
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