Melatonin protects against maternal diabetes-associated meiotic defects by maintaining mitochondrial function

Area of Science:

• Reproductive Biology
• Endocrinology
• Cell Biology

Background:

• Maternal diabetes negatively impacts oocyte quality.
• Strategies to prevent diabetes-induced oocyte damage are needed.
• Melatonin, an antioxidant, may improve oocyte quality.

Purpose of the Study:

• To investigate melatonin's protective effects on oocytes from diabetic mice.
• To explore the mechanisms underlying melatonin's action.
• To assess melatonin as a potential therapeutic strategy.

Main Methods:

• In vitro exposure of diabetic mouse oocytes to melatonin.
• Assessment of oocyte maturation, spindle/chromosome organization, reactive oxygen species (ROS) levels, cytosolic calcium (Ca2+), mitochondrial function, autophagy, and apoptosis.
• Analysis of TPX2 and pericentrin localization and LC3β expression.

Main Results:

• Melatonin improved oocyte maturation competence in diabetic mice.
• Melatonin corrected spindle and chromosome alignment defects by influencing TPX2 and pericentrin.
• Melatonin reduced ROS accumulation and increased cytosolic Ca2+ by preserving mitochondrial function.
• Melatonin reversed increased autophagy and apoptosis via decreased LC3β expression.

Conclusions:

• Melatonin supplementation protects oocytes from maternal diabetes-induced meiotic defects and quality decline.
• Melatonin's mechanisms involve antioxidant effects, improved mitochondrial function, and regulation of autophagy/apoptosis.
• Melatonin represents a promising strategy for improving oocyte quality in assisted reproductive technologies.