Di‐(2‐ethylhexyl) phthalate induces ferroptosis in prepubertal mouse testes via the lipid metabolism pathway

and MDA levels, accumulation of lipid reactive oxygen species, downregulation of GPX4, and upregulation of ACSL4 and LPCAT3 were reversed. Collectively, our findings suggested that aberrant lipid metabolism and ferroptosis may be involved in prepubertal DEHP exposure-induced testicular damage.