Ammonia-nitrogen is a common stress factor for aquatic organisms in their habitation environment, which is enriched in water due to high-density farming and environmental pollution. Ammonia nitrogen can enter fish body through gill, epidermis, digestive tract, and other tissues, causing fish ammonia poisoning. In the present study, juvenile blunt snout bream (average weight, 45 ± 5 g) were exposed to high concentrations of ammonia-nitrogen stress (25.0 ± 0.5 mg/L) for six different treatment times (0, 3, 6, 12, 24, 48, and 72 h); the tissue ultrastructure, mRNA levels of antioxidation system, and apoptosis patterns were studied. The antioxidant systems of malondialdehyde (MDA), catalase (CAT), acid phosphatase (ACP), and reduced glutathione (GSH) in various tissues were highly transcripted at 6 or 12 h (hpt) after treatment under high ammonia-nitrogen, which may play a role in preventing cells from being attacked by highly toxic reactive oxygen species (ROS). After 24 hpt, the antioxidant capacity threshold is breached, followed by the decline of antioxidant enzyme activity. Thus, with the prolonging of high ammonia-nitrogen processing time, ammonia-nitrogen stress caused irreversible damage of organs (gill, liver, and kidney). Furthermore, the expression of caspase-3 apoptotic pathway was highly induced in different tissues, implying the apoptotic system is activated, which causes extensive cell apoptosis in different tissues as shown using TUNEL analysis. In conclusion, we observed that, in response to acute ammonia-nitrogen stress, blunt snout bream enhances antioxidant capacity and cell apoptosis.