Selenium-induced alterations in ionic currents of rat cardiomyocytes

Area of Science:

• Cardiovascular Physiology
• Toxicology
• Cellular Electrophysiology

Background:

• Selenium is an essential trace element with complex biological roles.
• Chronic exposure to selenium compounds can lead to toxicity.
• Understanding selenium's effects on cardiac function is crucial for assessing health risks.

Purpose of the Study:

• To investigate the effects of chronic sodium selenite treatment on cardiac electrophysiology in rats.
• To examine the impact on ion channel currents, action potential, and contractile function.
• To explore potential correlations with metabolic changes and oxidative stress.

Main Methods:

• Rats were treated with sodium selenite (5 micromol/kg/day) for 4 weeks.
• Electrophysiological parameters including L-type Ca2+-current (ICaL), transient outward (Ito), inward rectifier (IK1), and steady state (Iss) K+-currents were measured.
• Contractile activity, action potential, and intracellular Ca2+ transients were assessed.
• Blood glucose, plasma insulin, and glutathione levels were analyzed.

Main Results:

• Sodium selenite increased blood glucose and decreased plasma insulin levels.
• Action potential duration was slightly prolonged without significant changes in spontaneous contraction or Ca2+ transients.
• Significant alterations in ICaL and Ito kinetics were observed, including slowed inactivation of ICaL and faster inactivation of Ito.
• Total charge carried by Ca2+ current increased by ~50%, while K+ currents decreased by ~50%.
• IK1 density was significantly inhibited, and oxidized glutathione levels increased.

Conclusions:

• Chronic selenium exposure alters cardiac ion channel kinetics and density, potentially leading to proarrhythmic effects.
• Observed metabolic and oxidative stress changes may be linked to selenium-induced cardiac dysfunction.
• These findings highlight the potential risks of chronic selenium supplementation on cardiovascular health.