Molecular and biochemical evidences on the protective effects of triiodothyronine against phosphine-induced cardiac and mitochondrial toxicity

Abdolghaffari, Amir Hossein; Baghaei, Amir; Solgi, Reza; Gooshe, Maziar; Baeeri, Maryam; Navaei-Nigjeh, Mona; Hassani, Shokoufeh; Jafari, Abbas Ali; Rezayat, Seyed Mehdi; Dehpour, Ahmad Reza; Mehr, Shahram Ejtemaei; Abdollahi, Mohammad

doi:10.1016/j.lfs.2015.07.026

Cited by 49 publications

(38 citation statements)

References 60 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The use of different therapeutic modalities was reported in the literature with varied degrees of success, including magnesium sulphate [13], N-acetyl cysteine [14], triiodothyronine [15], intra-aortic balloon pump [16], and extracorporeal membrane oxygenation as an assist device [8]. …”

Section: Discussionmentioning

confidence: 99%

Reversible Myocardial Injury and Intraventricular Thrombus Associated with Aluminium Phosphide Poisoning

Hangouche

Fennich

Alaika

et al. 2017

Case Reports in Cardiology

View full text Add to dashboard Cite

Aluminium phosphide (ALP) is widely used as a fumigant pesticide. In case of ALP poisoning, it is responsible for myocardial dysfunction, related to toxic myocarditis, and hemodynamic disorders. We report a case of a 28-year-old female who had intentionally ingested ALP and was admitted with cardiogenic shock. The transthoracic echocardiography (TTE) at the time of admission showed severe global myocardial hypokinesia with the presence of a giant left ventricular thrombus. Cardiovascular magnetic resonance (CMR) revealed extensive toxic myocarditis with a left ventricular systolic dysfunction. All cardiac lesions were reversible after symptomatic treatment, within 6 months. We aim, by reporting this case, to evidence the complete reversibility of cardiac injury due to aluminium phosphide poisoning documented by transthoracic echocardiography and cardiovascular magnetic resonance.

show abstract

Section: Discussionmentioning

confidence: 99%

Reversible Myocardial Injury and Intraventricular Thrombus Associated with Aluminium Phosphide Poisoning

Hangouche

Fennich

Alaika

et al. 2017

Case Reports in Cardiology

View full text Add to dashboard Cite

show abstract

“…In particular, animal studies indicated that AlP decreases the activity of complexes II and IV. It was also shown that administration of AlP can reduce cellular ATP levels . Moreover complexes I, II and IV activity were mitigated in patients with AlP ingestion .…”

Section: Mitochondrial Complexes: Role Of Melatonin and Aluminium Phomentioning

confidence: 94%

“…Unfortunately, administration of exogenous drugs, such as triiodothyronine, vasopressin, iron sucrose, sodium bicarbonate, digoxin, Mg nanoparticle, pralidoxime and N‐acetylcysteine, has not been complete effective therapeutic agents in the case of AlP‐induced cardiotoxicity. The lack of specific antidote and effective supportive care results in high mortality of this poison .…”

Section: Introductionmentioning

confidence: 99%

A review of the protective role of melatonin during phosphine-induced cardiotoxicity: focus on mitochondrial dysfunction, oxidative stress and apoptosis

Asghari

Abdollahi

Oliveira

et al. 2017

Journal of Pharmacy and Pharmacology

Self Cite

View full text Add to dashboard Cite

Objectives Acute poisoning with aluminium phosphide (AlP) is a major cause of mortality in developing countries. AlP mortality is due to cardiac dysfunction leading to cardiomyocyte death. The main mechanism is an inhibition of cytochrome c oxidase in the cardiomyocyte mitochondria, resulting in a decreased ATP production and oxidative stress. Unfortunately, the administration of exogenous drugs does not meet the desired requirements of an effective therapy. Melatonin is an amphiphilic molecule and can easily pass through all cellular compartments with the highest concentration recorded in mitochondria. It is known as a vigorous antioxidant, acting as a potent reactive oxygen species (ROS) scavenger. Our aim is to summarize the mechanisms by which melatonin may modulate the deteriorating effects of AlP poisoning on cardiac mitochondria. Key findings Melatonin not only mitigates the inhibition of respiratory chain complexes, but also increases ATP generation. Moreover, it can directly inhibit the mitochondrial permeability transition pore (mPTP) opening, thus preventing apoptosis. In addition, melatonin inhibits the release of cytochrome c from mitochondria to hinder caspase activation leading to cell survival. Summary Based on the promising effects of melatonin on mitochondria, melatonin may mitigate AlP-induced cardiotoxicity and might be potentially suggested as cardioprotective in AlP-intoxicated patients.

show abstract

“…The protocol used consisted of isocratic elution with tetrabutylammonium hydrogen sulfate (TBAHS) (4 mM) in potassium phosphate buffer (0.1 M; pH 5.5) and methanol (85:15 vol/vol). The flow rate was 1 mL/min for 20 minutes at 254 nm . The levels of ATP and ADP were quantified, after creating of standard curve, and the ratio was calculated.…”

Section: Methodsmentioning

confidence: 99%

Molecular mechanisms of action of styrene toxicity in blood plasma and liver

Niaz

Mabqool

Khan

et al. 2017

Environmental Toxicology

Self Cite

View full text Add to dashboard Cite

Styrene is an aromatic colorless hydrocarbon available in liquid form and highly volatile. In its pure form, it gives a sweet smell. The primary source of exposure in the environment is from plastic materials, rubber industries, packaging materials, insulations, and fiber glass and carpet industry. Natural sources of styrene include: few metabolites in plants which are transferred through food chain. The current study was designed to evaluate styrene toxicity, including: superoxide dismutase (SOD) and protein carbonyl, oxidative stress, glucose-6-phosphatase (G6Pase), glycogen phosphorylase (GP), and phosphoenolpyruvate carboxykinase (PEPCK) activities, adenosine triphosphate (ATP) to adenosine diphosphate (ADP) ratio, and changes in gene expressions such as glutamate dehydrogenase 1 (GLUD1), glucose transporter 2 (GLUT2), and glucokinase (GCK) in the rat liver tissue. For this purpose, styrene was dissolved in corn oil and was administered via gavage, at doses 250, 500, 1000, 1500, 2000, mg/kg/day per mL and control (corn oil) to each rat with one day off in a week, for 42 days. Plasma SOD and protein carbonyl of plasma were significantly up-regulated in 1000, 1500, and 2000 mg/kg/day styrene administrated groups (P < .001). In addition, styrene caused an increase in lipid peroxidation (LPO) and reactive oxygen species (ROS) in the dose-dependent manners in liver tissue (P < .001). Furthermore, the ferrous reducing antioxidant power (FRAP) and total thiol molecules (TTM) in styrene-treated groups were significantly decreased in liver tissue (P < .001) with increasing doses. In treated rats, styrene significantly increased G6Pase activity (P < .001) and down-regulated GP activity (P < .001) as compared to the control group. The PEPCK activity was significantly raised in a dose-dependent manner (P < .001). The ATP/ADP ratio of live cells was significantly raised by increasing the dose (P < .001). There was significantly an up-regulation of GLUD1 and GCK at 2000 mg/kg group (P < .01) and a down-regulation for GLUT2 at the same dose. While in the rest of group, GLUT2 showed up-regulation of relative fold change. By targeting genes such as GLUD1, GLUT2, and GCK, disruption of hepatic gluconeogenesis, glycogenolysis, and insulin secretory functions are obvious. The present study illustrates that induction of oxidative stress followed by changes in G6Pase, GP, and PEPCK activities and the genes responsible for glucose metabolism are the mechanisms of styrene's action in the liver.

show abstract

Molecular and biochemical evidences on the protective effects of triiodothyronine against phosphine-induced cardiac and mitochondrial toxicity

Cited by 49 publications

References 60 publications

Reversible Myocardial Injury and Intraventricular Thrombus Associated with Aluminium Phosphide Poisoning

Reversible Myocardial Injury and Intraventricular Thrombus Associated with Aluminium Phosphide Poisoning

A review of the protective role of melatonin during phosphine-induced cardiotoxicity: focus on mitochondrial dysfunction, oxidative stress and apoptosis

Molecular mechanisms of action of styrene toxicity in blood plasma and liver

Contact Info

Product

Resources

About