Fig. 8. Schematic diagram of arsenic-induced male reproductive toxicity and riboflavin protective function via Bmp4/Bmpr1α signaling (Created with BioGDP.com).

Both in vivo and in vitro experiments demonstrated that arsenic exposure induces male reproductive toxicity, primarily characterized by decreased sperm quality, impaired blood–testis barrier integrity, and inhibited proliferation of Sertoli cells or TM4 cells. Mechanistically, riboflavin mediates the binding of Bmp4 to Bmpr1α and participates in riboflavin metabolism, thereby effectively reversing these arsenic-induced adverse effects. Note: Upward red arrows (↑) represent upregulation or enhancement; downward black arrows (↓) represent downregulation or inhibition.