Abstract
The study was designed to determine the impact of acute toxicity of fumaronitrile exposure through tissue damaging, oxidative stress enzymes and histopathological studies in gills, liver and muscle cells of freshwater tilapia fish (Oreochromis mossambicus). In gill, liver, and muscle cells, biochemical indicators such as tissue damage enzymes (Acid Phosphatase (ACP), Alkaline Phosphatase (ALP), and Lactate Dehydrogenase (LDH)) and antioxidative enzymes (Superoxide Dismutase (SOD); Catalase (CAT); Glutathione-S-transferase (GST); Reduced Glutathione (GSH); Glutamate oxaloacetate transaminase (GOT) and Glutamate pyruvate transaminase (GPT) were quantified in the time interval of 30, 60 and 90 days exposure to the fumaronitrile. After 90 days, under 6 ppb exposure conditions, the acid phosphatase (ACP) levels of fish increased significantly in the gills (3.439 μmol/mg protein/min), liver (1.743 μmol/mg protein/min), and muscles (2.158 μmol/mg protein/min). After 90 days of exposure to the same concentration and days, ALP activity increased significantly in gills (4.354 μmol/mg protein/min) and liver (1.754 μmol/mg protein/min), but muscle cells had a little decrease in ALP activity (2.158 μmol/mg protein/min). The LDH concentration in gills following treatment with fumaronitrile over a period of 0-90 days was 3.573 > 3.521 > 2.245 μmol/mg protein/min over 30 > 60 > 90 days. However, at the same dose and treatment duration, a greater LDH level of 0.499 μmol/mg protein/min was found in liver and muscle cells. Histopathological abnormalities in the gills, liver, and muscle cells of treated fish were also examined, indicating that fumaronitrile treatment generated the most severe histological changes. The current study reveals that fumaronitrile exposure has an effect on Oreochromis mossambicus survival, explaining and emphasising the risk associated with this POP exposure to ecosystems and human populations.