Assessment of Acute Ammonia Stress on Growth Performance, Hematological, Serological, and Histopathological Changes in Grass Carp (<i>Ctenopharyngodon Idella</i>)

<i>Background:</i> Fish are a vital source of high-energy nutrition, especially for economically disadvantaged populations. Grass carp (<i>Ctenopharyngodon idella</i>), prized for their quality meat, are widely consumed worldwide including in Pakistan. However, environmental ammonia pollution from aquaculture poses significant risks to their health, impacting physiological functions, growth, and survival. Understanding ammonia toxicity is crucial for sustainable aquaculture and environmental protection. <i>Objectives: </i>This research aimed to investigate the toxicity of ammonium hydroxide on the growth, hematological parameters, and histopathological changes in gills of grass carp. <i>Methods: </i>Grass carp were exposed to various concentrations of ammonium hydroxide (0, 1, 1.5, and 2 mg/L) for a duration of 14 days in glass aquaria. Growth performance, hematological parameters (including Hb, RBC, MCHC, WBC, MCV, MCH, and cholesterol levels), and serological parameters (such as bilirubin, creatinine, uric acid, SGPT, and alkaline phosphate) were assessed. Histopathological analysis of the gills was conducted to observe any abnormalities. <i>Results: </i>The results revealed that increased concentrations of ammonium hydroxide led to retarded growth in grass carp, with the lowest growth rate observed in the experimental group exposed to 2 mg/L of ammonium hydroxide and the highest growth rate in the control group (0 mg/L). Hematological parameters indicated a significant decrease in Hb, RBC, MCHC, and WBC counts with increasing levels of ammonium hydroxide, while MCV, MCH, and cholesterol levels increased. Serological parameters showed elevated levels of bilirubin, creatinine, uric acid, SGPT (ALT), and alkaline phosphate with increasing ammonium hydroxide concentrations. Histopathological analysis of the gills revealed significant effects, including chloride cell hyperplasia, sideway swimming, hyperemia, epithelial lifting, curling of secondary lamellae, lamellar fusion, and shortening of secondary lamellae.