On the mechanisms of taurine in alleviating electrocardiographic, hemodynamic, and biochemical parameters following aluminum phosphide cardiotoxicity
Male
Membrane Potential, Mitochondrial
0301 basic medicine
0303 health sciences
Cardiotonic Agents
Phosphines
Taurine
Myocardium
Troponin I
Blood Pressure
Heart
Cardiotoxicity
Mitochondria
3. Good health
Electrocardiography
Oxidative Stress
03 medical and health sciences
Electron Transport Chain Complex Proteins
Heart Rate
Animals
Rats, Wistar
Aluminum Compounds
Creatine Kinase
DOI:
10.1016/j.fct.2021.112347
Publication Date:
2021-06-15T17:12:35Z
AUTHORS (13)
ABSTRACT
Aluminum phosphide (AlP) causes severe cardiotoxicity. Taurine has been chosen for the present study because of its positive known effects on cardiac injuries.To evaluate AlP-induced cardiotoxicity, the animals were divided into seven groups, including the control group, the taurine group (500 mg/kg), AlP with LD50 dose, AlP + taurine 20, 50, 100, and 200 mg/kg group. To assess cardiac hemodynamic parameters, Wistar rats received taurine intraperitoneally 60 min after AlP gavage. Cardiac hemodynamic parameters were evaluated for 180 min. To study biochemical parameters, 24 h after AlP treatment, the animals were sacrificed, and heart tissues were collected.ECG, BP, and HR abnormalities of AlP poisoning were improved by taurine treatment. AlP induced biochemical alterations including complexes I and IV activities, the ADP/ATP ratio, mitochondrial membrane potential, cytochrome C release, and oxidative stress biomarkers ameliorated by taurine. Moreover, taurine improved apoptosis, as well as lessened CK-MB and troponin I levels. Also, there were no significant changes between taurine 500 mg/kg and the control group in tests.The present findings showed that taurine could be a possible candidate for AlP cardiotoxicity treatment via the effect on mitochondrial electron transfer chain and maintaining intracellular ATP balance.
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