High Ammonia Nitrogen-Induced Reproductive Toxicity in Goldfish (Carassius auratus) Mature Ovary

Abstract

Ammonia nitrogen is one of the major pollutants in aquaculture. However, the mechanism of ammonia stress on ovarian development and follicular atresia is unknown. In this study, goldfish (Carassius auratus) were exposed to different ammonia concentrations, including 0 (control, C) and 50 mg/L (high, H) for 48 hr at 21 ± 0.5°C. Histology of the ovarian tissue sections revealed that the high ammonia concentrations inhibited the maturation of oocytes, and induced broken and wrinkled radiation bands, follicular membranes, and the accumulation of rod-shaped yolk particles. From the transcriptome data, a total of 1,405 differentially expressed genes (DEGs) were detected between H and C groups. Most DEGs were highly enriched in low-density lipoprotein particle-mediated signaling, oxidative stress-induced premature senescence, and ovarian steroidogenesis pathway. Furthermore, a total of 19 genes were selected and determined by quantitative real-time polymerase chain reaction (qRT-PCR). The changes in oxidative stress and antioxidant activity indicated the excessive accumulation of reactive oxygen species (ROS) in ovarian tissue. The ovarian apoptosis was induced in the H group. The downregulation of genes involved in the ovarian steroidogenesis pathway indicated that ammonia nitrogen stress prevented the synthesis of sexual hormones. These results suggest that high-concentration ammonia stress induces ovarian damage in goldfish, affecting its antioxidant function, leading to excessive ROS accumulation, ovarian apoptosis, and hindered steroid synthesis, adversely affecting reproductive performance.