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Acetyl-l-carnitine attenuates arsenic-induced liver injury by abrogation of mitochondrial dysfunction, inflammation, and apoptosis in rats.
Environ Toxicol Pharmacol. 2018 Mar; 58:11-20.ET

Abstract

Industrial and agricultural developments in recent years have resulted in the excessive discharge of arsenic into the environment, making arsenic toxicity a major worldwide concern. Oxidative stress is considered the primary mechanism for arsenic toxicity. The main objective of this study was to evaluate acetyl-l-carnitine's (ALC) protective ability against the arsenic-induced hepatotoxicity. For this purpose, male Wistar rats were distributed randomly into 5 groups of 8 rats each: control, arsenic (5 mg/kg) and arsenic plus ALC (5 mg/kg; 100, 200, 300 mg/kg). The animals were gavaged for 21 consecutive days. Liver tissue samples were extracted 24 h after the last treatment and were later analyzed for biochemical and histological alterations. The arsenic-induced oxidative damage was confirmed by elevation of malondialdehyde (MDA), a lipid peroxidation byproduct, as well as depletion in physiological antioxidant content such as superoxide dismutase (SOD) and catalase (CAT). Furthermore, alterations in mitochondrial functions including a significant decrease of mitochondrial outer membrane potential and reactive oxygen species (ROS) generation increase, mitochondrial swelling, release of cytochrome c and consequent activation of caspase-3 and caspase-9 and initiation of apoptosis, was observed following arsenic administration. Moreover, the inflammation was confirmed by the overexpression of inflammatory mediators such as NF-ĸB and IL-1 and IL-6. The present study demonstrated that ALC ameliorates arsenic-induced oxidative damage, mitochondrial dysfunction, apoptosis, inflammation and histological damage. ALC's protective features against arsenic hepatotoxicity may be due to this agent's antioxidant and anti-inflammatory properties as well as its stabilizing effects on mitochondrial function.

Authors+Show Affiliations

Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.Department of Anatomical Sciences, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran; Toxicology and Poisoning Research Centre, Tehran University of Medical Sciences, Tehran, Iran; Drug Design and Development Research Centre, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: omid@tums.ac.ir.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

29278859

Citation

Bodaghi-Namileh, Vida, et al. "Acetyl-l-carnitine Attenuates Arsenic-induced Liver Injury By Abrogation of Mitochondrial Dysfunction, Inflammation, and Apoptosis in Rats." Environmental Toxicology and Pharmacology, vol. 58, 2018, pp. 11-20.
Bodaghi-Namileh V, Sepand MR, Omidi A, et al. Acetyl-l-carnitine attenuates arsenic-induced liver injury by abrogation of mitochondrial dysfunction, inflammation, and apoptosis in rats. Environ Toxicol Pharmacol. 2018;58:11-20.
Bodaghi-Namileh, V., Sepand, M. R., Omidi, A., Aghsami, M., Seyednejad, S. A., Kasirzadeh, S., & Sabzevari, O. (2018). Acetyl-l-carnitine attenuates arsenic-induced liver injury by abrogation of mitochondrial dysfunction, inflammation, and apoptosis in rats. Environmental Toxicology and Pharmacology, 58, 11-20. https://doi.org/10.1016/j.etap.2017.12.005
Bodaghi-Namileh V, et al. Acetyl-l-carnitine Attenuates Arsenic-induced Liver Injury By Abrogation of Mitochondrial Dysfunction, Inflammation, and Apoptosis in Rats. Environ Toxicol Pharmacol. 2018;58:11-20. PubMed PMID: 29278859.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Acetyl-l-carnitine attenuates arsenic-induced liver injury by abrogation of mitochondrial dysfunction, inflammation, and apoptosis in rats. AU - Bodaghi-Namileh,Vida, AU - Sepand,Mohammad Reza, AU - Omidi,Ameneh, AU - Aghsami,Mehdi, AU - Seyednejad,Seyed Afshin, AU - Kasirzadeh,Sara, AU - Sabzevari,Omid, Y1 - 2017/12/12/ PY - 2017/09/23/received PY - 2017/12/10/revised PY - 2017/12/11/accepted PY - 2017/12/27/pubmed PY - 2018/8/28/medline PY - 2017/12/27/entrez KW - Acetyl-l-carnitine KW - Arsenic KW - Hepatic mitochondrial toxicity KW - Inflammation KW - Oxidative stress SP - 11 EP - 20 JF - Environmental toxicology and pharmacology JO - Environ Toxicol Pharmacol VL - 58 N2 - Industrial and agricultural developments in recent years have resulted in the excessive discharge of arsenic into the environment, making arsenic toxicity a major worldwide concern. Oxidative stress is considered the primary mechanism for arsenic toxicity. The main objective of this study was to evaluate acetyl-l-carnitine's (ALC) protective ability against the arsenic-induced hepatotoxicity. For this purpose, male Wistar rats were distributed randomly into 5 groups of 8 rats each: control, arsenic (5 mg/kg) and arsenic plus ALC (5 mg/kg; 100, 200, 300 mg/kg). The animals were gavaged for 21 consecutive days. Liver tissue samples were extracted 24 h after the last treatment and were later analyzed for biochemical and histological alterations. The arsenic-induced oxidative damage was confirmed by elevation of malondialdehyde (MDA), a lipid peroxidation byproduct, as well as depletion in physiological antioxidant content such as superoxide dismutase (SOD) and catalase (CAT). Furthermore, alterations in mitochondrial functions including a significant decrease of mitochondrial outer membrane potential and reactive oxygen species (ROS) generation increase, mitochondrial swelling, release of cytochrome c and consequent activation of caspase-3 and caspase-9 and initiation of apoptosis, was observed following arsenic administration. Moreover, the inflammation was confirmed by the overexpression of inflammatory mediators such as NF-ĸB and IL-1 and IL-6. The present study demonstrated that ALC ameliorates arsenic-induced oxidative damage, mitochondrial dysfunction, apoptosis, inflammation and histological damage. ALC's protective features against arsenic hepatotoxicity may be due to this agent's antioxidant and anti-inflammatory properties as well as its stabilizing effects on mitochondrial function. SN - 1872-7077 UR - https://www.unboundmedicine.com/medline/citation/29278859/Acetyl_l_carnitine_attenuates_arsenic_induced_liver_injury_by_abrogation_of_mitochondrial_dysfunction_inflammation_and_apoptosis_in_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1382-6689(17)30326-5 DB - PRIME DP - Unbound Medicine ER -