# Hepatoprotective role of ascorbic acid against fenvalerate-induced histopathological, ultrastructural, and antioxidant disruptions in Ctenopharyngodon idella

## TL;DR

The study shows that ascorbic acid protects the liver of Ctenopharyngodon idella fish from damage caused by fenvalerate, a pesticide.

## Contribution

This study demonstrates the hepatoprotective effects of ascorbic acid against fenvalerate-induced liver damage in Ctenopharyngodon idella.

## Key findings

- Fenvalerate causes oxidative stress and liver damage in Ctenopharyngodon idella.
- Ascorbic acid supplementation reduces antioxidant enzyme activity and liver pathology in fenvalerate-treated fish.
- Histopathological and ultrastructural analyses confirm the protective role of ascorbic acid.

## Abstract

Ctenopharyngodon idella, a herbivorous fish, is widely used in aquaculture to control aquatic weeds. Owing to its significant role, the present study investigates the protective effects of ascorbic acid (AA) against fenvalerate (FEN) toxicity in the liver of Ctenopharyngodon idella. Dietary AA supplementation (1000 mg/kg diet) was tested against 1.2 and 2 µg/L of FEN and fish were dissected on the 15th, 30th, and 60th day of the experiment. The results revealed a significant (p < 0.05) increase in liver antioxidant enzyme levels (superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, and reduced glutathione) on the 15th and 30th days of FEN treatment followed by a decrease on the 60th day as compared to control group. While as, the malondialdehyde level was elevated throughout the experiment. Histopathological analysis revealed severe liver damage in FEN-treated fish, with notable infiltration of sinusoids, necrosis, and pycnotic nuclei, resulting in a mean degree of tissue change (DTC) value of 117.12 ± 1.27 at 2 µg/L of FEN on the 60th day of the experiment. Transmission electron microscopy displayed significant anomalies, including glycogen depletion, fragmented rough endoplasmic reticulum, swollen mitochondria, loss of heterochromatin, and necrotic hepatocytes with disrupted cytoplasm. However, dietary AA supplementation significantly minimized antioxidant enzyme activity and reduced liver pathology in FEN-treated fish, demonstrating its hepatoprotective efficacy. The study concludes that AA supplementation is recommended in aquaculture systems to mitigate the adverse effects of FEN.

•FEN induces hepatotoxicity in C. idella, causing oxidative stress and liver damage.•Elevated SGOT, SGPT, and ALP levels indicate FEN-induced liver dysfunction.•AA supplementation mitigates FEN toxicity, demonstrating hepatoprotective effects.•AA’s antioxidant properties reduce oxidative stress and serum markers.•Histopathological analysis confirms AA’s protective role against FEN-induced liver damage.

FEN induces hepatotoxicity in C. idella, causing oxidative stress and liver damage.

Elevated SGOT, SGPT, and ALP levels indicate FEN-induced liver dysfunction.

AA supplementation mitigates FEN toxicity, demonstrating hepatoprotective effects.

AA’s antioxidant properties reduce oxidative stress and serum markers.

Histopathological analysis confirms AA’s protective role against FEN-induced liver damage.