Abstract
ABSTRACT This study determined the LC50-24 h value of sodium pyrithione (NaPT) on Cyprinus carpio at 102.7643 µg/L. Then, 60 healthy fish were randomly allocated into 6 exposure groups, each receiving varying levels of NaPT for different durations (control goup = 0% µg/L NaPT for 24 and 96 h; NaPT-10 = 10% of the LC50-24 h dose of NaPT for 24 and 96 h; NaPT-20 = 20% of the LC50-24 h dose of NaPT for 24 and 96 h). As a result, the increase in malondialdehyde (MDA) levels and the decrease in catalase (CAT), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) activities in the gill and liver tissue in both duration and dose groups were found to be statistically significant. In addition, NaPT increased serum tumour necrosis factor (TNF-α), interleukin-1 beta (IL-1β), interleukin-6 (IL-6) levels in both dose groups for both durations. The results revealed that NaPT exposure caused shortening of gill tissue lamellae and vacuolisation (separation) of the secondary lamellar epithelium. Likewise, NaPT exposure was responsible for vacuolisation and hepatocellular degeneration in liver tissue in hepatocytes. In conclusion, the toxicity study, antioxidant enzyme activities, cytokine immune response, and histopathological results indicate that NaPT has a toxic effect on the carp.
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