Nicotinamide mononucleotide protects ovarian function and oocyte developmental competence during chemotherapy

Area of Science:

• Reproductive biology
• Oncology
• Biochemistry

Background:

• Chemotherapy, specifically cyclophosphamide (CTX), can cause ovarian dysfunction and infertility in female cancer patients.
• Existing fertility preservation methods have limitations, necessitating novel, non-invasive strategies.
• Nicotinamide adenine dinucleotide (NAD+) plays a role in DNA repair and apoptosis, making its precursors potential candidates for ovarian protection.

Purpose of the Study:

• To investigate the protective effects of nicotinamide mononucleotide (NMN), an NAD+ precursor, against cyclophosphamide (CTX)-induced ovarian damage.
• To evaluate NMN's potential as a non-invasive fertility preservation strategy during chemotherapy.

Main Methods:

• Female C57 mice received saline, CTX, or CTX with NMN supplementation for 14 days.
• Ovarian reserve, oocyte quality, and embryo development were assessed.
• NAD+ levels, reactive oxygen species (ROS), DNA damage, and apoptosis were measured in ovarian tissue and blastocysts.

Main Results:

• NMN supplementation increased ovarian NAD+ levels, improved ovarian reserve, and enhanced endocrine function.
• NMN reduced ROS, DNA damage, and apoptosis in both ovarian tissue and blastocysts.
• Embryo development rates (two-cell and blastocyst formation) and blastocyst cell counts were improved with NMN treatment.

Conclusions:

• NMN demonstrates significant protective effects against CTX-induced reproductive toxicity.
• NMN represents a promising non-invasive strategy for fertility preservation in cancer patients undergoing chemotherapy.
• The protective mechanisms may involve key genes like Banp, Rbm47, and Sgk1.