Nitrite (NIT) is one of the most common toxic compounds in aquaculture. However, the effects of NIT exposure on the reproductive capabilities of aquatic animals remain largely unknown. This study explored the consequences of NIT exposure on the ovarian tissues of Procambarus clarkii and revealed that it significantly reduced ATP content and gonadosomatic index (GSI), causing metabolic imbalance, reactive oxygen species (ROS) accumulation, increased oxidative stress, and altered antioxidant enzyme activity. Pathological investigation revealed a decrease in the number of oogonia and oocytes, as well as an increase in vacuolated and apoptotic cells in the ovary. Differentially expressed genes (DEGs) and gene set enrichment analysis (GSEA) revealed that genes related to oxidative stress, apoptosis, and autophagy were significantly upregulated, whereas genes involved in ovarian development and energy metabolism were downregulated. These findings suggested that NIT exposure not only caused oxidative stress and abnormal energy metabolism, but also activated autophagy and apoptosis in the ovarian cells. In addition, the Nrf2/Keap1 (nuclear factor erythroid 2-related factor 2/Kelch-like ECH-associated protein 1) signaling pathway was found to be activated. Nrf2 knockdown inhibited antioxidant, apoptotic, and autophagy activities while increasing the expression of genes related to reproduction and nutrient metabolism. Selenomethionine (Se-Met) treatment alleviated NIT exposure-induced ovarian damage by elevating antioxidant capacity, superoxide dismutase, and catalase activities and reducing the levels of H2O2, malondialdehyde, glutathione, and ROS. In addition, Se-Met improved the anti-inflammatory and antioxidant stress responses by activating the Nrf2/Keap1 pathway and attenuating NIT-induced ovarian toxicity. Overall, this study provides a novel approach for maintaining ovarian homeostasis after NIT exposure.