Selenium supplementation modulates apoptotic processes in thyroid follicular cells

Area of Science:

• Molecular Biology
• Cell Biology
• Nutritional Science

Background:

• Selenium (Se) is an essential micronutrient with critical roles in human health.
• Thyroid function is influenced by various physiological and pathological processes.
• Understanding selenium's molecular effects on thyroid cells is crucial for its health implications.

Purpose of the Study:

• To investigate the molecular effects of selenium supplementation on rat thyroid follicular cells (FRTL5).
• To evaluate selenium's impact on cell growth, mortality, proliferation, and apoptosis.
• To determine selenium's role in preventing endoplasmic reticulum (ER) stress-induced apoptosis.

Main Methods:

• Utilized the well-differentiated rat thyroid follicular cell line FRTL5.
• Assessed cell growth rate, mortality, and proliferation.
• Analyzed mRNA levels of pro-apoptotic (p53, Bim) and anti-apoptotic (NF-kB, Bcl2) factors.
• Evaluated ER-stress apoptosis markers, including caspase activity and protein cleavage.

Main Results:

• Selenium supplementation significantly improved FRTL5 cell growth rate.
• Selenium reduced the proportion of cell death and modulated key apoptotic gene expression.
• High doses of sodium selenite (Na-Se) protected cells from tunicamycin-induced ER-stress apoptosis, evidenced by maintained membrane integrity and reduced caspase activity.

Conclusions:

• Selenium supplementation positively influences thyroid follicular cell growth and survival.
• Selenium modulates both pro- and anti-apoptotic pathways in thyroid cells.
• These findings provide molecular evidence for selenium's protective role against ER-stress-induced apoptosis in the thyroid, relevant to its overall physiopathology.