Citotoxicity of Fipronil on Hepatocytes Isolated from Rat and Effects of Its Biotransformation

Guelfi, Marieli; Maioli, Marcos A.; Tavares, Marco Aurélio; Mingatto, Fábio Ermínio

doi:10.1590/s1516-89132015060298

Cited by 16 publications

(10 citation statements)

References 42 publications

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“…The protective mechanisms toward oxidative stress mainly through balances mediated by non-enzymatic and enzymatic antioxidants 71 . In current study, the decrease in SOD and GPx activities of rats subjected to FIP might be due to the excess production of O 2 that is rapidly transformed by SOD and GPx to H 2 O 2 and water, respectively as reported in the liver of pregnant rats and their offspring due to the inadequate ROS detoxification produced by FIP in hepatocyte 33 , 66 .…”

Section: Discussionmentioning

confidence: 57%

“…Several studies suggested that redox homeostasis disturbance was triggered during FIP toxicity was because of high ROS production 33 , 64 , 65 . Hepatotoxicity induced by FIP in this study might be due to increased levels of MDA and NO (the indicator of LPO) because of the high reactive oxygen metabolites production especially the hydroxyl radicals 33 , 66 , LPO play role in the disruption of the integrity of cellular membranes and implicated in liver injuries 67 . ROS can target cell membranes and other cellular molecules, resulting in protein oxidation, lipid peroxidation, caspase3 activation, and DNA damage 33 , 68 , leading to cell dysfunction 69 , 70 .…”

Section: Discussionmentioning

confidence: 71%

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The potential ameliorative impacts of cerium oxide nanoparticles against fipronil-induced hepatic steatosis

Wasef

Nassar

El‐Sayed

et al. 2021

Sci Rep

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Fipronil (FIP) is a phenylpyrazole insecticide that is commonly used in agricultural and veterinary fields for controlling a wide range of insects, but it is a strong environmentally toxic substance. Exposure to FIP has been reported to increase the hepatic fat accumulation through altered lipid metabolism, which ultimately can contribute to nonalcoholic fatty liver disease (NAFLD) development. The present study aimed to examine the function of cerium oxide nanoparticles (CeNPs) in protecting against hepatotoxicity and lipogenesis induced by FIP. Twenty-eight male albino rats were classified into four groups: FIP (5 mg/kg/day per os), CTR, CeNPs (35 mg/kg/day p.o.), and FIP + CeNPs (5 (FIP) + 35 (CeNPs) mg/kg/day p.o.) for 28 consecutive days. Serum lipid profiles, hepatic antioxidant parameters and pathology, and mRNA expression of adipocytokines were assessed. The results revealed that FIP increased cholesterol, height-density lipoprotein, triacylglyceride, low-density lipoprotein (LDL-c), and very-low-density lipoprotein (VLDL-c) concentrations. It also increased nitric oxide (NO) and malondialdehyde (MDA) hepatic levels and reduced glutathione peroxidase (GPx) and superoxide dismutase (SOD) enzyme activities. Additionally, FIP up-regulated the fatty acid-binding protein (FABP), acetyl Co-A carboxylase (ACC1), and peroxisome proliferator-activated receptor-alpha (PPAR-α). Immunohistochemically, a strong proliferation of cell nuclear antigen (PCNA), ionized calcium-binding adapter molecule 1 (Iba-1), cyclooxygenase-2 (COX-2) reactions in the endothelial cells of the hepatic sinusoids, and increased expression of caspase3 were observed following FIP intoxication. FIP also caused histological changes in hepatic tissue. The CeNPs counteracted the hepatotoxic effect of FIP exposure. So, this study recorded an ameliorative effect of CeNPs against FIP-induced hepatotoxicity.

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Section: Discussionmentioning

confidence: 57%

Section: Discussionmentioning

confidence: 71%

The potential ameliorative impacts of cerium oxide nanoparticles against fipronil-induced hepatic steatosis

Wasef

Nassar

El‐Sayed

et al. 2021

Sci Rep

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“…These findings indicated that FPN triggers intrinsic apoptosis via the mitochondrial signaling pathway that is initiated by the generation of ROS [56,58]. The mechanism of FPN toxicity involved its effect on mitochondrial bioenergetics and an alteration in calcium homeostasis, which led to a decrease in ATP synthesis with consequent cell death by necrosis [30]. Looking for potentially neuroprotective agents from natural products could attenuate oxidative stress-induced neurotoxicity might be helpful in the prevention and treatment of neurodegenerative disorders [63].…”

Section: Discussionmentioning

confidence: 99%

“…The first group (I) served as control; hence animals were orally given olive oil. The second group (II) was orally treated with FPN only (10.5 mg/kg BW) approximately 1/10 LD 50 [30]. The third group (III) was treated with combination of FPN (10.5 mg/kg BW) and TL methanol extract (TLE) (100 mg/kg BW) and finally the fourth group (IV) was orally treated with dissolved TLE only (100 mg/kg BW).…”

Section: Methodsmentioning

confidence: 99%

The Terminalia laxiflora modulates the neurotoxicity induced by fipronil in male albino rats

et al. 2019

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The extensive use of fipronil (FPN) may trigger hazards to more than insects. The present investigation was carried out to evaluate the abrogating role of Terminalia laxiflora (TL) methanol extract (TLE) against the neurotoxic effects provoked by FPN. Fourty male albino rats were assigned into four equal groups. The first group served as control, the second one was orally administered FPN (10.5 mg/kg BW), the third group was given combination of FPN and TLE) (100 mg/kg BW), and the fourth one was orally given TLE. Our findings highlighted the efficacy of TLE as a neuroprotectant through a significant reduction in malondialdehyde (MDA) content by 25.8%, elevations of the reduced glutathione (GSH) level, catalase (CAT,) and superoxide dismutase (SOD) activities by 30.9, 41.2, and 48.2% respectively. Consequently, the relative mRNA levels of both Bax and caspase-3 were down-regulated by 40.54% and caspase-3 by 30.35% compared with the control group. Moreover, restoration of the pathological tissue injuries were detected. In conclusion, TLE proved to be a potent neuroprotective agent against the FPN-induced toxicity.

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“…This synthetic chemical has great efficiency in controlling resistant/tolerant pest, which justifies its widespread use in several countries [6], although it is highly toxic for some animal species [12].…”

Section: Introductionmentioning

confidence: 99%

Histopathological changes in the liver and thyroid of mice (Mus musculus) caused by the acaricides: fipronil and thymol

Cunha¹,

Matos²,

Pereira³

et al. 2017

J Histol Histopathol

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The control of tick Rhipicephalus (Boophilus) microplus, that has the cattle as preferential host, has been performed using products based on different chemical substances. However, the indiscriminate use of these products has caused the selection of resistant populations and damages to the environment, contaminating the soil and water. Tickcides, like fipronil (synthetic chemical) and thymol (natural chemical), are applied on cattle through aspersion, causing the death of the ectoparasites. Nevertheless, the effects of these products on nontarget organisms have not been thoroughly investigated. Thus, this study evaluated the morphology of the liver and thyroid of female Mus musculus mice, divided into 5 treatment groups/5 individuals each, exposed to fipronil (2%) and thymol (2 mg/mL) through aspersion baths. After exposure, the mice were euthanized with anaesthetic overdose and dissected for organ removal. The results showed that both fipronil and thymol caused morphological alterations in the organs: cytoplasmic vacuolation, cell death characteristics in hepatocyte nuclei and structural disorganization of the thyroid gland. Along with body weight measurement, the results suggest that the morphological alterations would be a systemic response of the organism to the toxic action of these products, regardless their origin (synthetic of natural).

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Citotoxicity of Fipronil on Hepatocytes Isolated from Rat and Effects of Its Biotransformation

Abstract: The aim of this study was to characterize the mechanism of toxicity of fipronil on hepatocytes isolated from the rat and the effect of its biotransformation on the toxicological potential.

Cited by 16 publications

References 42 publications

The potential ameliorative impacts of cerium oxide nanoparticles against fipronil-induced hepatic steatosis

The potential ameliorative impacts of cerium oxide nanoparticles against fipronil-induced hepatic steatosis

The Terminalia laxiflora modulates the neurotoxicity induced by fipronil in male albino rats

Histopathological changes in the liver and thyroid of mice (Mus musculus) caused by the acaricides: fipronil and thymol

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