The m6A modification mediates the imbalance of mitochondrial homeostasis and apoptosis induced by Benzo[b]fluoranthene in mouse spermatocytes: mitophagy versus mitochondrial damage - PubMed
7 hours ago
- #m6A modification
- #Reproductive toxicity
- #Mitochondrial homeostasis
- The study investigates the male reproductive toxicity of Benzo[b]fluoranthene (BbF) and its mechanisms.
- BbF exposure disrupts mitochondrial homeostasis in mouse spermatocytes, leading to reproductive toxicity.
- Mitochondrial damage occurs via the p53/PGC-1α/TFAM signaling pathway, impairing biogenesis and oxidative phosphorylation.
- PINK1/Parkin-associated mitophagy is activated as a compensatory response to mitigate cellular damage.
- YTHDF2 downregulation by BbF slows Trp53 mRNA degradation, increasing p53 levels and exacerbating mitochondrial damage.
- METTL3 plays a protective role by enhancing Mark4 mRNA stability, promoting PINK1/Parkin-associated mitophagy.
- The balance between mitochondrial damage and mitophagy determines the outcome of BbF-induced toxicity.