In vivo studies on hepato-renal impairments in freshwater fish Cyprinus carpio following exposure to sublethal concentrations of sodium cyanide.

Reactive oxygen species is an inevitable composite of aerobic systems that could channelize their lethality by imparting oxidative stress under a stressful environment. Cyanide is an important environmental toxicant that could be responsible in the resulting detrimental health issues of aquatic fauna. The present effort investigates the possibilities of hepato-renal damage in freshwater fish Cyprinus carpio following exposure to sublethal concentrations of sodium cyanide (NaCN). Fish were exposed to 0.1 mg/L of NaCN for 10 days (E1) and 20 days (E2) and were further subjected to recovery for 14 days (R) in NaCN-free medium. Liver tissue exhibited a significant decline in activity of catalase, superoxide dismutase, glutathione peroxidase, and glutathione S-transferase enzymes in exposed fish, unlike in control (C). Subsequent levels of lipid peroxidation elevation at 'E1' and 'E2' suggested oxidative damage to hepatocytes. This was further confirmed through a histopathological evaluation which indicated important findings like lymphocytic infiltration and necrosis in liver and tubular and glomerular degeneration in renal organ. The investigation suggests biochemical and histopathological alterations in fish following exposure to NaCN. Nevertheless, fish upon the recovery period were known to exhibit incomplete recuperation which was indicated by partial restoration tendencies under biochemical and histopathological factions. The study clearly implicated the role of NaCN in emphasizing its toxicity to C. carpio, further suggesting lack of recovery transition at a limited tenure of 14 days. The study might contribute in the course of regulatory surveillance and monitoring of aquatic bodies and may also reflect the possibilities of NaCN contamination during aquaculture practices. Graphical Abstract ᅟ.