Mitochondrial Dysfunction Plays a Relevant Role in Heart Toxicity Caused by MeHg

Area of Science:

• Environmental Health
• Toxicology
• Cardiovascular Science

Background:

• Methylmercury (MeHg) is a public health concern, primarily known for neurological effects.
• Cardiovascular impacts of MeHg exposure are less understood.
• Investigating MeHg's cardiotoxicity is crucial for comprehensive risk assessment.

Purpose of the Study:

• To evaluate the cardiotoxicity of a cumulative methylmercury dose in mice.
• To investigate MeHg's effects on cardiac mitochondrial function and proteins.
• To identify specific cardiovascular changes induced by MeHg exposure.

Main Methods:

• Mice received a cumulative dose of 70 mg/kg methylmercury over 14 days (MeHg70 group).
• Cardiac mitochondrial function was assessed using oxygraphy.
• In vivo assessments included ergometry, electrocardiography, and echocardiography.

Main Results:

• MeHg exposure reduced oxygen consumption and impaired mitochondrial complexes II and V efficiency.
• Mice showed decreased running tolerance and increased atrial natriuretic peptide mRNA.
• Electrocardiogram revealed lower heart rate and prolonged ventricular depolarization/repolarization.
• Echocardiography showed reduced left ventricular ejection fraction and wall thickness.

Conclusions:

• Oral methylmercury intake significantly impairs cardiac function and oxidative metabolism.
• MeHg exposure leads to measurable cardiotoxic effects in mice.
• Monitoring MeHg levels and cardiac function in exposed populations is recommended.