Molecular and biochemical evidence on the protection of cardiomyocytes from phosphine-induced oxidative stress, mitochondrial dysfunction and apoptosis by acetyl-l-carnitine

Baghaei, Amir; Solgi, Reza; Jafari, Abbas Ali; Abdolghaffari, Amir Hossein; Golaghaei, Alireza; Asghari, Mohammad Hossein; Baeeri, Maryam; Ostad, Seyed Nasser; Sharifzadeh, Mohammad; Abdollahi, Mohammad

doi:10.1016/j.etap.2015.12.019

Cited by 38 publications

(22 citation statements)

References 35 publications

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“…Vitamin E decreased the fatality rate [ 53 ] and exerted more marked effects when co-administered with NAC [ 52 ]. T3 [ 54 ], vasopressin [ 54 ] and ALCAR [ 63 ] were suggested to improve AlP-related alterations in cardiovascular function, ATP levels and apoptosis. Based on in vitro studies, 6-aminonicotinamide showed protective activity in hepatocytes [ 60 ].…”

Section: Discussionmentioning

confidence: 99%

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Antidotes for aluminum phosphide poisoning – An update

et al. 2018

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Aluminum phosphide (AlP), an inexpensive solid fumigant, is frequently used for grain conservation despite its alleged high toxicity. Increased utilization of AlP for agricultural and non-agricultural purposes during the last four decades has resulted in increment of AlP-attributed poisoning numbers. Moreover, due to its limitless accessibility in developing countries, AlP has been increasingly used for suicide. Moisture-exposed AlP undergoes a chemical reaction producing phosphine gas, which in turn inhibits cytochrome oxidase and impedes cellular oxygen consumption. Lethality remains elevated reaching rates of >50% and no effective antidote is available. Nevertheless, experimental and clinical studies suggested that magnesium sulfate, melatonin, N-acetylcysteine, glutathione, sodium selenite, vitamin C and E, triiodothyronine, liothyronine, vasopressin, milrinone, Laurus nobilis L., 6-aminonicotinamide, boric acid, acetyl-L-carnitine and coconut oil, may serve as antidotes by reducing the deleterious oxidative properties of AlP. This article reviews the afore-mentioned chemicals suggested to specifically treat AlP poisoning and discusses their protective mechanisms and main outcomes.

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Section: Discussionmentioning

confidence: 99%

“…Effects of acetyl-L-carnitine (ALCAR; 100, 200, and 300 mg/kg, IP) on AlP-induced toxicity were investigated in a rodent model with regard to mitochondrial respiratory chain activity, ATP production, oxidative stress and cellular apoptosis/necrosis [ 63 ]. ALCAR significantly ameliorated oxidative stress ( i.e.…”

Section: Acetyl-l-carnitinementioning

confidence: 99%

Antidotes for aluminum phosphide poisoning – An update

et al. 2018

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“…This result in agreement with Kariman et al (2012) and Mehrpour et al (2012) who found decrease in TAC in ALP studied patients. Several experimental studies reported that ALP could cause oxidative stress by production of oxygen free radicles, lipid peroxidation and impairment of mitochondrial electron transport chain resulting in decrease in TAC (Hsu et al, 2002Nath et al, 2011and Baghaei et al, 2016).These studies were supported with another study done by Halvaei et al (2017) who reported that there was decrease in TAC after ALP exposure indicating oxidative stress which was improved after administration of vitamin E as an antioxidant.…”

Section: Discussionmentioning

confidence: 54%

Assessment of the Role of Total Antioxidant Capacity and Troponin I as Possible Predictors for Phosphides -Induced Cardiotoxicity

Wahab

Shalaby

Awady

et al. 2020

Ain Shams Journal of Forensic Medicine and Clinical Toxicology

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Background: Metal phosphides are type of rodenticides that are extremely lethal with low safety and high mortality rates. They are commonly used as a powerful suicidal tool in Egypt and developing countries due to its low price and easy availability. Heart is a significant target organ of acute metal phosphides toxicity, causing myocardial damage and myocarditis. Aim: The study aimed to evaluate usefulness of total antioxidant capacity (TAC) and troponin I as predictive biomarkers for phosphides induced oxidative stress and cardiotoxicity among patients admitted to the Poison Control Center Ain Shams University Hospitals (PCC-ASUH). Methods and results: A prospective study included patients of both sexes presented to the PCC-ASUH with acute metal phosphides poisoning during six months period from July to December 2017. The demographic, intoxication and clinical data were collected for every patient. On admission investigations included electrocardiogram (ECG) in addition to TAC and troponin I levels. Outcome was also recorded. This study was conducted on 188 patients of both sexes with acute metal phosphides poisoning. The patients were classified according to the Poisoning Severity Score (PSS) into three groups; mild, moderate and severe. TAC value was significantly decreased in patients who developed cardiovascular manifestations and ECG abnormalities. Serum troponin I value was significantly higher in patients who developed cardiovascular manifestations and ECG abnormalities. Conclusion: The current study concluded that TAC and troponin I levels could be useful in predicting development of oxidative damage, cardiotoxicity and mortality after acute metal phosphides poisoning. Recommendations: The present study recommended the use of TAC and troponin I as useful markers for prediction of cardiotoxicity and mortality in patients with acute metal phosphides poisoning.

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“…The main physiologic role of L-carnitine is involvement in fat and energy metabolism by mediating the transport of long-chain free fatty acids (LCFAs) across the mitochondrial membrane for -oxidation [17] and ATP synthesis and exerts lipotrophic / lipolytic effects in a variety of cardiovascular diseases including atherosclerosis and stroke [17]. Aside from this leading task, LC supplementation has been reported to be associated with several health benefits such as regulation of carbohydrate metabolism and insulin sensitivity, mitigation of lipid peroxidation (LPo) and oxidative stress (OS), synthesis of heat shock proteins (HSPs), enhancement of the immune system and cytoprotection [18][19][20][21][22]. The mitochondrial antioxidant/nutrient acetyl-L-carnitine (ALC), with its iron-chelating antioxidant energizing protective activities and with its trophic effects, at optimal doses, can be an effective and safe prevention strategy for PD, offering the possibility of new and innovative therapeutic strategies for brain aging and several agerelated NDDs.…”

Section: Carnitine Synthesis and Function: L-carnitinementioning

confidence: 99%

Neuroprotective Epigenetic and DNA Damage Repairing Molecular Mechanisms of L-Carnitine and its Congeners against Aging and Age-Related Neurodegenerative Diseases

Ponnusamy¹

2017

10.21522/TIJBMS

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Aging is an ubiquitous biological phenomena characterized by ever-increasing susceptibility to diseases due to increased oxidative stress (OS) and an ultimate severe non-repairable membrane molecular and mitochondrial damages coupled with energy (ATP) depletion. L-Carnitine (β-hydroxy-γ-trimethyl amino butyrate) and its congeners plays an essential role in mitochondrial ATP synthesis while being a powerful anti-inflammatory antioxidant and an organic, non-ionic bi-phasic osmolytes. L-carnitine exerts antimutagenic and genome stabilizing effects by increasing mitochondrial metabolism, anneals DNAstrand breaks and enhances genome stability by modulating histones and DNA-repairing enzymes. Poly (ADP-ribose) polymerase-1 (PARP-1) is an abundant nuclear enzyme and normally functions in DNA damage repair mechanism acts as a double-edged sword, which anneals mild repairable DNA damages, but extensive PARP-1 activation can promote cell death through processes involving energy depletion in severe OS. It has been reported that, severe oxidative stress-mediated extensive non-repairable DNA damage can over-activate PARP-1 and consumes enormous NAD + and consequently ATP, culminating in cell dysfunction or necrosis by autocatalysis of PARP-1 and caspases. The DNA damage associated with OS known to activate DNA repair proteins, including PARP-1, an important biomarker of brain aging and age-related neurodegenerative diseases. This study delineates the neuroprotective epigenetic and DNArepairing molecular mechanisms of the iron-chelating anti-inflammatory genome stabilizing antioxidant ergogenic aid L-Carnitine and its congeners against selected degenerative diseases such as Parkinson's disease (PD), Alzheimer's disease, Amyotrophic Lateral Sclerosis (ALS) and Multiple sclerosis (MS).

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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

Cited by 38 publications

References 35 publications

Antidotes for aluminum phosphide poisoning – An update

Antidotes for aluminum phosphide poisoning – An update

Assessment of the Role of Total Antioxidant Capacity and Troponin I as Possible Predictors for Phosphides -Induced Cardiotoxicity

Neuroprotective Epigenetic and DNA Damage Repairing Molecular Mechanisms of L-Carnitine and its Congeners against Aging and Age-Related Neurodegenerative Diseases

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