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In the present investigation, hepatic oxidative stress induced by fipronil was evaluated in male mice. We also investigated whether pretreatment with antioxidant vitamins E and C could protect mice against these effects. Several studies conducted in cell lines have shown fipronil as a potent oxidant; however, no information is available regarding its oxidative stress inducing potential in an animal model. Out of 8 mice groups, fipronil was administered to three groups at low, medium, and high dose based on its oral LD50 (2.5, 5, and 10 mg/kg). All three doses of fipronil caused a significant increase in the serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) level with concomitant increase in the absolute and relative weight of liver. High dose of fipronil caused significant down-regulation in the hepatic mRNA expression of superoxide dismutase 1 (SOD1) and catalase (0.412 ± 0.01 and 0.376 ± 0.05-fold, respectively) as well as an increase in the lipid peroxidation (LPO). Also, decrease in the activity of antioxidant enzymes; SOD, catalase, and glutathione-S-transferase (GST) and the content of nonantioxidant enzymes; glutathione and total thiol were recorded. Histopathological examination of liver revealed dose dependant changes such as severe fatty degeneration and vacuolation leading to hepatocellular necrosis. Prior administration of vitamin E or vitamin C against fipronil high dose caused decrease in lipid peroxidation and increased activity of antioxidant enzymes. Severe reduction observed in functional activities of antioxidant enzymes was aptly substantiated by down-regulation seen in their relative mRNA expression. Thus results of the present study imply that liver is an important target organ for fipronil and similar to in vitro reports, it induces oxidative stress in the mice liver, which in turn could be responsible for its hepatotoxic nature. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1147-1158, 2016.

T-2 toxin is one of the most potent cytotoxic and food-borne mycotoxins. Most experimental studies on the T-2 toxin have been performed at extremely low doses (ppb level). However, several field reports of contaminated feed have shown concentration of T-2 toxin to be as high as ≥20 ppm. Therefore, the impact of high dose T-2 toxin (20 ppm) after subacute exposure was investigated in an experimental setup with respect to growth performance, oxidative stress, and detailed pathomorphology in young male Wistar rats. Furthermore, to see the effect of such a high dose on the accumulation of T-2 toxin, its residues in various organs were quantified by high-performance thin-layer chromatography (HPTLC). Apart from obvious clinical toxicosis, rats in the toxin-fed group showed significant hemato-biochemical alterations and increased levels of biological markers of oxidative stress with concomitant decrease in levels of serum and tissue catalase and superoxide dismutase. These alterations were strongly supported by histopathological changes, such as hyperkeratosis and hyperplasia of the squamous gastric mucosa, oxidative damage to hepatocytes, atrophy of the thymus and spleen, and overall decrease in the spermatogenic activity of testes. An economical, simple, reliable, and quick method for the detection and quantification of T-2 toxin residues by HPTLC is also reported here. No residual T-2 toxin was detected in any of the organs tested, suggesting that T-2 toxin does not accumulate in tissues even at such a high exposure level.

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