Lithium Treatment Induces Cardiac Dysfunction in Mice.

Area of Science:

• Cardiovascular toxicology
• Pharmacology
• Nephrology
• Hepatology

Background:

• Lithium (Li) salts are essential mood stabilizers for bipolar disorder.
• Increasing use of Li in electronics raises concerns about its toxicity.
• Potential cardiotoxic effects of Li warrant further investigation.

Purpose of the Study:

• To investigate the long-term effects of Li carbonate on cardiac, hepatic, and renal systems in mice.
• To assess Li-induced cardiotoxicity, including electrical activity, morphology, function, and molecular pathways.
• To evaluate multi-organ toxicity using histopathology.

Main Methods:

• Oral administration of Li carbonate to C57BL/6J mice for 12 weeks.
• Evaluation of cardiac electrical activity, morphology, and function.
• Histopathological assessment of heart, liver, and kidney tissues.

Main Results:

• Li treatment resulted in impaired systolic function and ventricular repolarization.
• Mice exhibited increased susceptibility to arrhythmias under adrenergic stimulation.
• Histopathology revealed cardiomyocyte hypertrophy, ERK pathway modulation, and minor tissue damage in Li-treated mice, with alterations in liver and kidney tissues.

Conclusions:

• Lithium exhibits cardiotoxic effects at therapeutic dosages.
• Li treatment induces histopathological changes in the liver and kidney.
• The developed mouse model can be utilized for testing Li-induced cardiotoxicity treatments.