Mitochondrial-targeted ROS scavenging by melatonin rescues 1-nitropyrene-induced defects in oocyte quality

Area of Science:

• Reproductive Toxicology
• Environmental Health
• Mitochondrial Biology

Background:

• 1-nitropyrene (1-NP) is a toxic environmental contaminant impacting reproductive health.
• Mechanisms of 1-NP's detrimental effects on oocyte quality are not fully understood.
• Melatonin, an antioxidant, may protect reproductive systems from oxidative damage.

Purpose of the Study:

• Investigate 1-NP's effects on mouse oocytes.
• Evaluate melatonin's protective potential against 1-NP toxicity.
• Elucidate the protective mechanisms of melatonin.

Main Methods:

• Exposure of mouse oocytes to 1-NP and melatonin.
• Transcriptomic sequencing to analyze gene expression.
• Assessment of oocyte maturation, fertilization, and development.
• Mitochondrial function and oxidative stress assays.
• Epigenetic modification analysis.

Main Results:

• 1-NP exposure impaired oocyte maturation, fertilization, and preimplantation development.
• 1-NP altered gene expression, leading to defective mitochondrial transcript clearance, dysfunction, and oxidative stress.
• 1-NP disrupted epigenetic modifications.
• Melatonin co-treatment ameliorated 1-NP-induced damage, restoring oocyte quality and developmental competence.
• Mito-TEMPO improved oocyte maturation and mitochondrial function in 1-NP exposed oocytes.

Conclusions:

• Melatonin protects mouse oocytes from 1-NP toxicity primarily by targeting mitochondria and reducing reactive oxygen species (ROS).
• Melatonin alleviates oxidative stress and restores oocyte quality and developmental competence.
• This highlights a potential therapeutic strategy against environmental reproductive toxicants.