Flubendiamide, a widely used diamide insecticide, is increasingly detected in aquatic ecosystems due to agricultural runoff, posing risks to non-target organisms such as fish. The present study investigates the acute effects of flubendiamide on liver histopathology in Labeo rohita. Fingerlings were divided into three experimental groups Control, LC?, and LC?? and exposed to the predetermined concentration of flubendiamide for 96 hrs under controlled laboratory conditions. Histological evaluation revealed several pathological alterations, including hepatocyte necrosis, vacuolation, sinusoidal dilation, nuclear pyknosis, blood congestion, and disruption of hepatic cords in LC?, and LC?? group. Tissue degeneration increased with concentration, indicating dose-dependent hepatotoxicity. These findings demonstrate that flubendiamide induces substantial structural damage to hepatic tissue, compromising metabolic and detoxification functions in fish. The study highlights the ecological risks associated with indiscriminate pesticide use and underscores the need for stringent monitoring of agricultural runoff into aquatic habitats.
Introduction
Pesticides are major environmental pollutants that, despite supporting agricultural productivity, pose serious risks to non-target organisms when used excessively. Aquatic ecosystems are particularly vulnerable due to pesticide runoff and persistence, and fish—important both ecologically and as a food source—readily absorb these chemicals, making them sensitive indicators of environmental contamination. The liver, as the primary organ for detoxification, is especially susceptible to pesticide-induced damage, and histopathological analysis is a reliable tool for assessing such toxicity.
This study evaluates the hepatotoxic effects of the insecticide flubendiamide on the freshwater fish Labeo rohita following acute exposure. Fish were exposed for 96 hours to LC? (7 mg L?¹) and LC?? (12 mg L?¹) concentrations, determined through toxicity bioassays. Liver tissues were processed using standard histological techniques and examined microscopically.
Results showed normal liver architecture in control fish, while exposed groups exhibited dose-dependent pathological changes. Fish at the LC? level showed mild to moderate liver damage, including disorganized hepatic cords, cytoplasmic vacuolation, sinusoidal dilation, vascular congestion, and pyknotic nuclei, indicating early cellular stress. At the LC?? concentration, liver damage was severe, with extensive hepatocellular degeneration, necrosis, hemorrhage, pronounced vacuolation, and destruction of tissue architecture.
The discussion attributes these alterations to oxidative stress, lipid peroxidation, mitochondrial dysfunction, and impaired antioxidant defenses induced by flubendiamide exposure. The progression from mild degeneration to severe necrosis demonstrates concentration-dependent hepatotoxicity, consistent with findings from similar studies on pesticide exposure in fish.
Conclusion
The present investigation demonstrates that acute exposure to the insecticide flubendiamide induces significant histopathological alterations in the liver of the freshwater fish Labeo rohita. Structural changes including cytoplasmic vacuolation, degeneration of hepatocytes, disorganization of hepatic cords, sinusoidal dilation, congested blood vessels, nuclear pyknosis, necrosis, and hemorrhagic lesions were observed, with severity increasing in a concentration-dependent manner. These pathological responses indicate impairment of liver function and disruption of cellular integrity, likely associated with oxidative stress and metabolic toxicity induced by flubendiamide. The study clearly reveals that even short-term sublethal exposure can adversely affect hepatic architecture, suggesting potential long-term ecological risks to fish health.
Considering the ecological and aquaculture importance of Labeo rohita, the findings highlight the necessity for careful regulation of flubendiamide usage near aquatic ecosystems and continued biomonitoring to minimize pesticide contamination. Further research focusing on chronic exposure, biochemical markers, antioxidant responses, and recovery potential is recommended to better evaluate environmental safety and toxicity thresholds.
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