Mechanism in bradycardia induced by Trimethyltin chloride: Inhibition activity and expression of Na+/K+-ATPase and apoptosis in myocardia.

doi:10.2131/jts.45.549

Paper

Mechanism in bradycardia induced by Trimethyltin chloride: Inhibition activity and expression of Na+/K+-ATPase and apoptosis in myocardia.

Published 2020 · Zhenzhong Liu, Zhiqiang Tian, Jiaqi Lv

The Journal of toxicological sciences

Q3 SJR score

8

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1

Influential Citations

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Abstract

Trimethyltin chloride (TMT) is a stabilizer by-product in the process of manufacturing plastic, which is a kind of very strong toxic substance, and has acute, cumulative and chronic toxicity. TMT may cause bradycardia in patients with occupational poisoning, the mechanism of which has not been reported. This study explored the mechanism of TMT resulting in bradycardia of C57BL/6 mice. TMT was administered to mice to measure heart rate, serum succinate dehydrogenase (SDH) level, and myocardial Na+/K+-ATPase activity and expression. The effects of TMT on myocardial apoptosis were observed by changing the expressions of caspase-3, Bax and Bcl-2 in myocardium. It was found that the heart rate and SDH activity in serum of mice gradually decreased with the increase of TMT dose compared with the control group. The activity and the expression of Na+/K+-ATPase in the heart tissue of mice exposed to TMT was measured and gradually decreased with the increase of dose and time. We measured the expression of Bcl-2, Bax, caspase-3 and cleaved caspase-3 in the heart tissues of TMT exposed mice and found that the expressions of Bax, caspase-3 and cleaved caspase-3 increased and the expressions of Bcl-2 decreased in the heart tissues of the TMT-exposed mice at different doses. With the extension of TMT exposure time, the expression of Bax and caspase-3 increased and the expression of Bcl-2 decreased in the heart tissues of TMT exposed mice. Our findings suggest the mechanisms of TMT resulting in bradycardia may be associated with the inhibited activity and decreased content of Na+/K+-ATPase, thus further leading to the changes of Bcl-2, Bax, caspase-3 and cleaved caspase-3 in the mice's ventricular tissues.

Non-RCT

Animal Study

Study Snapshot

Trimethyltin chloride (TMT) causes bradycardia in mice by inhibiting the activity and decreasing the content of Na+/K+-ATPase, leading to changes in Bcl-2, Bax, caspase-3, and cleaved caspase-3 in ventricular tissues

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Paper

Mechanism in bradycardia induced by Trimethyltin chloride: Inhibition activity and expression of Na+/K+-ATPase and apoptosis in myocardia.

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References

Citations

Ameliorative Effects of Betanin in Mice with Trimethyltin-Induced Pancreatic and Hepatocytic Alterations

Betanin effectively alleviates pancreatic and hepatocytic alterations caused by trimethyltin exposure, preventing pancreatic beta cell damage, maintaining liver glycogen content, and reducing inflammation.

Trimethyltin chloride induces oxidative damage and apoptosis in chicken liver

TMT exposure in chickens leads to oxidative stress and apoptosis, causing liver injury.

Effects of Dityrosine on Lactic Acid Metabolism in Mice Gastrocnemius Muscle During Endurance Exercise via the Oxidative Stress-Induced Mitochondria Damage.

Dityrosine, found in commercial food, decreases lactic acid metabolism in the gastrocnemius muscle during endurance exercise by inducing oxidative stress and mitochondrial damage.

Trimethyltin chloride exposure induces apoptosis and necrosis and impairs islet function through autophagic interference.

TMT exposure induces apoptosis and necrosis in pancreatic cells through autophagy disturbance, impairing pancreatic function at different concentrations.

Quantitative Proteomics Reveals the Neurotoxicity of Trimethyltin Chloride on Mitochondria in the Hippocampus of Mice.

TMT exposure in mice leads to cognitive disorders and mitochondrial respiratory chain abnormalities, potentially promoting apoptosis through impaired transport and increased apoptosis.

Bidirectional regulatory effects of Cordyceps on arrhythmia: Clinical evaluations and network pharmacology

Cordyceps has a positive effect on treating arrhythmia, with its main mechanism being the regulation of adrenergic signaling in cardiomyocytes and the PI3K-Akt signaling pathway.

TMT induces apoptosis and necroptosis in mouse kidneys through oxidative stress-induced activation of the NLRP3 inflammasome.

TMT can induce oxidative stress, activate the NF-B pathway, and cause apoptosis and necroptosis in mouse kidneys through inflammasomes.