In vertebrates, the core mechanisms that control gametogenesis are largely multiple, complex, successive, and orchestrated by intrinsic and extrinsic factors. However, age, health status, and hormonal activity are important factors for good fertility; other intangible intracellular molecular mechanisms that manage oocyte development are still unclear. The present study was designed to elucidate the ultrastructure changes in the ovary in response to its exposure to zinc oxide nanoparticles (ZnO-NPs) and to explore the role of autophagy and apoptosis during egg maturation and ovulation on the fertility of female zebrafish. In our study, ZnO-NPs could induce cytotoxicity in the maturing oocyte by activating autophagy and apoptosis in a caspase-dependent manner and could induce oxidative stress by generating reactive oxygen species (ROS) that elevated the mutated ovarian tP53 protein. Simultaneously, necroptosis developed, mimicking the features of apoptosis and necrosis. ZnO nanoparticles (LC50: 3.48 mg/L) were synthesized and characterized. Zebrafish were exposed to 0.69 mg/L ZnO-NPs for 15/30 days. Tissues were analyzed via histology, TEM, and Western blot (p53, VASA, Pgr, Caspase-3). Zinc levels were measured by FAAS. Data were analyzed by one-way ANOVA (*p < 0.05). Collectively, ZnO-NPs created a suitable necrotic environment that led to follicular developmental retardation that altered oocyte ovulation and reduced fecundity of female zebrafish.