Ammonia is one of the most common aquatic pollutants. To analyze the effect of ammonia exposure on the glutathione redox system, we investigated the levels of hydrogen peroxide (H2O2) and glutathione, and transcription and activities of glutathione-related enzymes in liver and gills of FFRC strain common carp (Cyprinus carpio L.) exposed to 0, 10, 20, and 30 mg/L of ammonia. The results showed that H2O2 content reached a maximum level at 48 h of exposure in the liver of fish. In gills, H2O2 increased rapidly at 6 h and reached to maximum levels at 24 h of exposure, indicating that gills experienced oxidative stress earlier than the liver of fish exposed to ammonia. Reduced glutathione (GSH) content and reduced glutathione/oxidized glutathione (GSH/GSSG) ratio increased significantly within 24 h of exposure. Meanwhile, the transcription and activities of glutathione S-transferase (GST) and glutathione reductase (GR) increased significantly in the liver, and glutathione peroxidase (GSH-Px) and GST increased in the gills of fish exposed to ammonia. Malondialdehyde (MDA) content kept at a low level after exposure to low concentration of ammonia, but increased significantly after exposure to 30 mg/L ammonia for 48 h along with a decrease in GSH content and GSH/GSSG ratio. These data showed that the glutathione redox system played an important role in protection against ammonia-induced oxidative stress in the liver and gills of FFRC strain common carp, though the defense capacity was not able to completely prevent oxidative damage occurring after exposure to higher concentration of ammonia. This research systematically studied the response of the glutathione redox system to ammonia stress and would provide novel information for a better understanding of the adaptive mechanisms of fish to environmental stress.