Fipronil induced oxidative stress in kidney and brain of mice: Protective effect of vitamin E and vitamin C

Badgujar, Prarabdh C.; Pawar, Nitin N.; Chandratre, Gauri A.; Telang, A.G.; Sharma, Anil Kumar

doi:10.1016/j.pestbp.2014.10.013

Cited by 104 publications

(68 citation statements)

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“…From previous literature, it was clear that fipronil produces oxidative stress; however all these studies were conducted in an in vitro system or particularly cell lines (Lassiter et al, ; Ki et al, ). Although there are couple of recent reports on oxidative stress inducing potential of fipronil in an animal model (Tukhtaev et al, ; Badgujar et al, ); however, its effect on liver oxidative stress has not yet been reported. Since fipronil is used both commercially and in home applications, its use warrants caution owing to serious environmental and public health concerns (Jennings et al, ; Tingle et al, ).…”

Section: Discussionmentioning

confidence: 99%

Fipronil induced oxidative stress involves alterations in SOD1 and catalase gene expression in male mice liver: Protection by vitamins E and C

et al. 2015

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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.

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Section: Discussionmentioning

confidence: 99%

Fipronil induced oxidative stress involves alterations in SOD1 and catalase gene expression in male mice liver: Protection by vitamins E and C

et al. 2015

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“…Although FPN toxicity has been thought to be restricted to insect neuronal transmitter receptors, several reports have shown that FPN is a potent toxicant affecting environmental species populations and, potentially, humans (Tingle et al, 2003;Overmyer et al, 2007). Recent studies have reported that FPN exposure significantly induces lipid peroxidation and oxidative stress in the kidney and brain of mice (Badgujar et al, 2015), as well as disruption of thyroid function in rats (Julien et al, 2009) and cytotoxicity in human hepatocytes (Das et al, 2006). Furthermore, we previously showed that FPN induces neuronal cell death in human neuroblastoma SH-SY5Y cells via an apoptotic pathway mediated by reactive oxygen species (ROS) and inflammatory response (Lee et al, 2011;Park et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Progressive loss of nigrostriatal dopaminergic neurons induced by inflammatory responses to fipronil

Park

Koh

2016

Toxicology Letters

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“…Free radicals seek out an electron to regain their stability and vitamin C donates electrons to free radicals such as hydroxyl and superoxide radicals and ultimately quenches their reactivity [21]. Most fish species cannot synthesize vitamin C, and have to depend on external sources to meet their needs.…”

Section: Introductionmentioning

confidence: 99%

“…The vitamin C requirement for normal growth and survival is quite low; however, a higher level is required to improve the stress resistance of fish [22]. Few studies have evaluated the protective role of vitamin C against oxidative stress induced by metals and pesticides in fish [21,23,24].…”

Section: Introductionmentioning

confidence: 99%

Methylmercury-Induced Oxidative Stress in Rainbow Trout (Oncorhynchus mykiss) Liver: Ameliorating Effect of Vitamin C

Mozhdeganloo

Jafari

Koohi

et al. 2015

Biol Trace Elem Res

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The present study was undertaken to evaluate methylmercury-induced alterations in hepatic enzymes and oxidative stress markers in liver tissue of rainbow trout (Oncorhynchus mykiss) by using a perfusion method, and to explore possible protective effect of vitamin C against these alterations. Forty-eight fish were divided into six groups containing control, test, and amelioration groups. The liver of fish in the test groups were exposed to different doses of methylmercury, i.e., 0.6, 1.2, and 2.4 μg L(-1), respectively, for 120 min. In the amelioration group, liver was treated with vitamin C (17.2 μg L(-1)) along with high dose (2.4 μg L(-1)) of methylmercury. The results of the present study showed that exposure with 0.6, 1.2, and 2.4 μg L(-1) of methylmercury significantly increased (p < 0.05) hepatic enzyme activities (alanine transaminase (ALT), aspartate transaminase (AST), and Lactate dehydrogenase (LDH)) and malondialdehyde (MDA) level, as a marker of lipid peroxidation. On the other hand, the concentration of reduced glutathione (GSH) and total antioxidant capacity of the liver decreased (p < 0.05) in the methylmercury-exposed groups when compared to the control group. Pearson's correlation analysis revealed a positive correlation between MDA concentration and ALT, AST, and LDH activities in the methylmercury groups, suggesting that the enhanced lipid peroxidation may be linked to hepatic damage caused by methylmercury. Treatment with vitamin C in methylmercury-exposed group led to a significant decrease (p < 0.05) in MDA concentration and hepatic enzyme activities and significant increase (p < 0.05) in levels of GSH and total antioxidant capacity. The values of measured parameters in the methylmercury + vitamin C group were comparable to those of the control group. The results of the present study demonstrated that methylmercury exposure induces oxidative stress in the liver of rainbow trout and treatment with vitamin C can protect fish liver against this oxidative insult.

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Fipronil induced oxidative stress in kidney and brain of mice: Protective effect of vitamin E and vitamin C

Cited by 104 publications

References 35 publications

Fipronil induced oxidative stress involves alterations in SOD1 and catalase gene expression in male mice liver: Protection by vitamins E and C

Fipronil induced oxidative stress involves alterations in SOD1 and catalase gene expression in male mice liver: Protection by vitamins E and C

Progressive loss of nigrostriatal dopaminergic neurons induced by inflammatory responses to fipronil

Methylmercury-Induced Oxidative Stress in Rainbow Trout (Oncorhynchus mykiss) Liver: Ameliorating Effect of Vitamin C

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