Abstract
Chemotherapy-induced reproductive toxicity remains a formidable off-target consequence of anticancer regimens, creating a critical barrier to the preservation of ovarian endocrine and gametogenic function in female patients. This review dissects the molecular and cellular cascades that underpin chemotherapy-driven ovarian insult—including DNA double-strand breaks, mitochondrial depolarization, accelerated primordial follicle activation, and oxidative stress—and critically evaluates emerging cytoprotective modalities. By synthesizing current mechanistic insights with pre-clinical and early-phase clinical data, we outline innovative strategies poised to mitigate ovarian damage without compromising oncological efficacy. GRAPHICAL ABSTRACT: [Image: see text]