Acute ammonia exposure combined with heat stress impaired the histological features of gills and liver tissues and the expression responses of immune and antioxidative related genes in Nile tilapia.

ABSTRACT

Ammonia exposure can be considered more stressful for aquatic animals when it coincides with high temperature. This study was conducted to detect the effects of ammonia exposure and heat stress and their interactions on the histological features of gills and liver tissues and the expression responses of immune and antioxidative related genes in Nile tilapia. Thus, 180 fish were divided into four groups (triplicates), where the first and third groups were kept in clean water without total ammonium nitrogen (TAN) exposure. At the same time, the second and fourth groups were exposed to 5 mg TAN/L. After seven days, the water temperature was raised in the third (without ammonia toxicity) and fourth (exposed with 5 mg TAN/L) groups up to 32 °C and kept under these conditions for 24 h. While the first (without ammonia toxicity) and second (exposed with 5 mg TAN/L) groups were kept under optimum water temperature (27.28 °C) then gills and liver tissues were dissected. Marked upregulation of keap1 was seen in the gills of fish exposed to ammonia/heat stress. The expression of mRNA levels for nrf2, nqo-1, cat, and gpx genes were downregulated in all stressed groups, with the lowest was recorded in the ammonia/heat stress group. The transcription of ho-1 was upregulated in the ammonia and heat stress groups while downregulated in the ammonia/heat stress group. The transcription of the complement C3 gene was downregulated in the livers of heat stress and ammonia/heat stress groups, while the lysozyme gene was downregulated in the ammonia/heat stress group. The mRNA expression levels of nf-κB, il-1ß, and tnf-α genes were higher in the ammonia group than in the heat stress group. The highest transcription level of nf-κB, il-1ß, tnf-α, il-8, and hsp70 genes and the lowest C3 and lysozyme genes were observed in fish exposed to ammonia/heat stress. The co-exposure to ammonia with heat stress triggered degeneration of primary and secondary gill filaments with telangiectasia and vascular congestion of secondary epithelium while, the liver showed hepatic vascular congestion and visible necrotic changes with nuclear pyknosis. In conclusion, the combined exposure of ammonia and heat stress induced oxidative stress, immunosuppression, and inflammation in Nile tilapia.