Assessment of fipronil toxicity on wistar rats: A hepatotoxic perspective

Abstract

Extensive pesticide application has contributed to environmental contamination globally, imposing adverse health effects on non-target organisms. Need for an understanding of cellular response following pesticide exposure is, therefore, paradigmatic for elucidating perturbations occurring within biological systems. The present investigation was aimed to examine safe and toxic dose level of a persistent, synthetic, phenylpyrazole based insecticide, Fipronil (FPN) on rat liver. Experimental animals were divided into four groups and gavaged with 0.0 (control), 32.33 (high), 12.12 (medium) and 6.46 mg/kg body weight/day (low dose) of FPN for 90 days. While results for liver catalase and glutathione S-transferase indicated significant changes in high and medium dose groups, the superoxide dismutase and glutathione peroxidase activity suggested significant changes in all exposed groups as compared to control. Elevated levels of liver malondialdehyde reflected oxidative damage potential under the exposed groups but remained insignificant for low dose. Histologically, structural irregularities with findings like impaired portal vein and hypertrophy of hepatocytes were prominent under all the exposed groups. The FT-IR based spectral investigation further revealed changes in absorption patterns and peak intensities in rats exposed to FPN. Significant elevation was also noticed in liver enzymes; alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase in rat serum suggesting the toxicity in dose -dependent pattern. Based on the outcome, it could be ascertained that the toxicity of FPN is certain at high and medium dose levels but remains ambiguous at a low dose of 6.46 mg/kg body weight/day. The current upshots serve as a preliminary report thereby advising the farming community against the usage of FPN insecticide.

Keywords: Antioxidants; Fipronil; Hepatotoxicity; Necrosis; Pesticide.

Graphical abstract

Fig. 1

Changes in body weight gain of male rats under control and exposed group.

Fig. 2

Photomicrograph showing sections of rat liver of Control (0.0 mg/kg BW/day) a: Hepatocytes (H), Portal Vein (PV), Blood sinusoids (BS), Hepatic Artery (HA), Bile Duct (BD), interlobular Connective Tissue; rats exposed to High dose (32.33 mg/kg BW/day) b: Damaged Bile Duct (BD), Ruptured Portal Vein (PV), dilated blood sinusoids (BS), Damaged Hepatic Artery (HA), Hypertrophy of Hepatocytes (H), Disrupted Connective Tissue (CT), Focal Necrosis (F); rats exposed to medium dose (12.12 mg/kg BW/day) c: Mild Dilation of Blood Sinusoids (BS), Partial clogging of Bile Duct (BD) and Portal Vein (PV), Damaged Hepatic Artery (HA) and Connective Tissue (CT), Hypertrophy of Hepatocytes (H), Stagnation of Bile (B), mild Vacuolation (V), Focal Necrosis (F); rats exposed to with low dose (6.46 mg/kg BW/day) d: Hypertrophy of Hepatocytes (H), Clogged Portal Vein (PV), (H and E staining, 200 X).

Fig. 3

Photomicrograph showing control and FPN exposed sections of rat liver; notice intact hepatocytes, blood sinusoids, portal vein, and bile duct in (a): Control (0.0 mg/kg BW/day); Degenerated hepatocytes, damaged portal vein, bile duct and necrotized area around portal vein (b): High dose- 32.33 mg/kg BW/day, c: Medium dose- 12.12 mg/kg BW/day and (d): Low dose- 6.46 mg/kg BW/day (H and E staining, processed with ImageJ, 200 X).

Fig. 4

Co-added and overlaid infrared spectra (4000–500 cm⁻¹ spectral region) of liver tissue for the control (0.0) and groups treated with high (32.33), medium (12.12) and low (6.46 mg/kg BW) dose of FPN.