Role of selenium and vitamin C in mitigating oxidative stress induced by fenitrothion in rat liver

Milošević, Marija; Paunović, Milica G.; Matić, Miloš; Ognjanović, Branka I.; Saičić, Zorica S.

doi:10.1016/j.biopha.2018.06.132

Cited by 36 publications

(13 citation statements)

References 42 publications

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“…For example, exposure of rats to phoxim resulted in decreases in liver GSH levels and total antioxidant capacity, while it increased liver weight . In contrast, fenitrothion administration in rats led to reductions in liver weight, and decreased activities of SOD, CAT and GSH levels in the liver . The present study demonstrated that exposure to 8:2 FTOH caused liver weight increases, while CAT and SOD activities in the liver decreased.…”

Section: Discussionsupporting

confidence: 48%

8:2 Fluorotelomer alcohol causes immunotoxicity and liver injury in adult male C57BL/6 mice

Wang

Kong

et al. 2018

Environmental Toxicology

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8:2 Fluorotelomer alcohol (8:2 FTOH) is widely used in houseware and industrial goods and is ubiquitous in the surrounding environment. 8:2 FTOH has been linked to hepatoxicity, nephrotoxicity, and reproductive toxicity, as well as endocrine-disrupting effects. However, as of yet, the research regarding immunotoxicity of 8:2 FTOH remains largely limited. In the present study, adult male C57BL/6 mice were administered with 10, 30, and 100 mg/kg/d 8:2 FTOH by gavage for 28 days to investigate its immunotoxicity in vivo. The results showed that exposure to 8:2 FTOH caused increases in liver weight and histological changes in the liver, including vacuolation, cell swelling, immune cell infiltration, karyopyknosis and nuclear swelling. No histological change in either the spleen or the thymus was observed after administration of 8:2 FTOH. In addition, exposure to 8:2 FTOH reduced the concentration of IL-1β in serum, and mRNA levels of IL-1β, IL-6, and TNF-α in both the thymus and spleen. CXCL-1 mRNA expression was downregulated in both the liver and thymus after 8:2 FTOH administration, while only IL-1β mRNA expression was upregulated in the liver. Moreover, the exposure of primary cultured splenocytes to 8:2 FTOH inhibited the ConA-stimulated proliferation of splenocytes at concentrations of 30 and 100 μM, and the LPS-stimulated proliferation of splenocytes at 100 μM. Furthermore, 8:2 FTOH inhibited the level of secreted IFN-γ in ConA-stimulated splenocytes. The results obtained in the study demonstrated that 8:2 FTOH posed potential immunotoxicity and liver injury in mice. Our findings will provide novel data for the health risk assessment of 8:2 FTOH. K E Y W O R D S 8:2 FTOH, immunotoxicity, liver injury, mice, oxidative stress 1 | INTRODUCTION Fluorotelomers, as fluorocarbon-based oligomers or telomers, have various applications in food packaging, home furnishings, fire-fighting foams, surfactants, textiles, adhesives, waxes, polishes, and leather. 1 It was reported that the market size of fluorotelomers was 26.5 kt in 2015, and its annual growth rate is estimated to be 12.7%. 2 Among fluorotelomers, fluorotelomer alcohol (FTOH) products dominate global consumption; these products reportedly made up approximately 32% of the overall volume of fluorotemomers in 2013. 3 8:2 FTOH is the most abundant FTOH homologue and is ubiquitous in the environment. 4 Chen et al. 5 detected FTOHs in several wastewater treatment plants in China, and the study also found that 8:2 FTOH was the primary FTOH in the influent, secondary effluent, and sludge, with the concentrations ranging from 2.10 to 11.0 ng/L, 3.05 to 12.4 ng/L, and 0.36 to 1.91 ng/g dry weight, respectively. Bach et al. 6 assessed 14 perfluorinated compounds (PFCs) in water samples in France and found that the concentrations of 8:2 FTOH were 117 ng/L and 213 ng/L in tap and surface water, respectively. Additionally, 8:2 FTOH was commonly detected in food contact materials (FCMs). For example, 8:2 FTOH was detected in most Chinese and American FCM samples at concentra...

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Section: Discussionsupporting

confidence: 48%

8:2 Fluorotelomer alcohol causes immunotoxicity and liver injury in adult male C57BL/6 mice

Wang

Kong

et al. 2018

Environmental Toxicology

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“… Fakhri-Bafghi et al (2016) have found selenium-based drugs have protective effects on the toxicity of three common OP compounds to human erythrocyte in vitro . In addition, Na 2 SeO 3 combined with VitC can reduce the toxic damage of OP compounds to the human body, but the effect of using Na 2 SeO 3 alone is not obvious ( Milošević et al, 2018 ). Although selenium protein or selenides have intrinsic biological activities ( Alim et al, 2019 ), their safe doses in vivo are small, and they are prone to toxicity, limiting the application of traditional seleno compounds ( Watanabe et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: Amorphous Selenium Nanoparticles Improve Vascular Function in Rats With Chronic Isocarbophos Poisoning via Inhibiting the Apoptosis of Vascular Endothelial Cells

Zhu

Zhi

et al. 2021

Front. Bioeng. Biotechnol.

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AimThis study aimed to investigate the preventive effect and possible mechanism of amorphous selenium nanoparticles (A-SeQDs) on isocarbophos induced vascular dysfunction.MethodsA-SeQDs was made by auto redox decomposition of selenosulfate precursor. Male rats were given isocarbophos (0.5 mg/kg/2 days) by intragastric administration for 16 weeks to induce vascular dysfunction. During the course, A-SeQDs (50 mg/kg/day) was added to the water from week 5. Then, the rats were killed to observe and test the influence of A-SeQDs on the vascular dysfunction induced by isocarbophos. Finally, human umbilical vein endothelial cells (HUVECs) were treated with 10% DMEM of isocarbophos (100 μM) for 5 days to detect the related indexes. Before the use of isocarbophos treatment, different drugs were given.ResultsA-SeQDs could reduce total carbon dioxide, MDA, VCAM-1, ICAM-1, IL-1, and IL-6 while increasing oxygen saturation, NO content, and SOD activity in rats. A-SeQDs also resulted in relatively normal vascular morphology, and the expression of sodium hydrogen exchanger 1 (NHE1) and caspase-3 decreased in rats. Furthermore, in HUVECs treated with isocarbophos, A-SeQDs maintained mitochondrial membrane potential, inhibited the cleaved caspase-3 expression, and released cytochrome c from mitochondria to cytosol.ConclusionA-SeQDs can inhibit the apoptosis of HUVECs through the mitochondrial pathway, and effectively treat the impairment of vascular endothelial function caused by isocarbophos, which is NHE1-dependent.

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“…Here, the consumption of reduced GSH via the activity of free radical hunter may be reflected as the primary reason for its reduction to protect the renal tissues from OS induced by DNPs 57 and/or FNT 14 . Subsequently, the decline in the renal GST activity may be attributed to the utilization of GSH, in general, and particularly due to the direct binding of DNPs 57 containing PAHs together with FNT 58 and/or its metabolites with GST. Another possible mechanism for the inhibition of GST activity is the involvement of this enzyme in the detoxification of cellular injury to combat the cell from the oxidative damage induced by ROS/RNS after intoxication with DNPs 17 and/or FNT 59 .…”

Section: Discussionmentioning

confidence: 99%

Linseed ameliorates renal apoptosis in rat fetuses induced by single or combined exposure to diesel nanoparticles or fenitrothion by inhibiting transcriptional activation of p21/p53 and caspase‐3/9 through pro‐oxidant stimulus

Ibrahim

Abdelgaid

El-Desouky

et al. 2021

Environmental Toxicology

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Gestational exposure to environmental pollutants can induce oxidative injury and apoptosis since the fetal organs are sensitively vulnerable to these chemicals. In this work, we have investigated the renal anti‐apoptotic efficiency of linseed (LS) against the oxidative stress‐mediated upregulation of the fetal apoptosis‐related genes following the prenatal intoxication with diesel nanoparticles (DNPs) and/or fenitrothion (FNT). A fifty‐six timed‐pregnant rats were equally divided to eight groups; control, LS (20% in diet), DNPs (0.5 mg/kg by intratracheal inoculation), FNT (3.76 mg/kg by gavage), DNPs+FNT, LS + DNPs, LS + FNT, and LS + DNPs+FNT. The transmission electron microscope analysis revealed the spherical shape of diesel particles with a homogeneous nanosized range (20–92.3 nm) and the crystallinity was confirmed by electron diffraction microscopy. Administration of DNPs and/or FNT significantly increased fetal renal malondialdehyde, nitric oxide, and glutathione reductase as compared with the control group. However, they declined the level of glutathione together with the activities of glutathione peroxidase, glutathione‐S‐transferase, superoxide dismutase, and catalase. Furthermore, DNPs and/or FNT elicited many histopathological changes in fetal renal cells, markedly up‐regulated apoptosis‐related gene expressions (p53, p21 caspase‐3, and caspase‐9), and evoked DNA breaks as detected by comet assay. Interestingly, LS supplementation significantly ameliorated the disturbances in oxidant/antioxidant biomarkers, downregulated the apoptosis gene expressions, and alleviated DNA damage alongside renal cell architecture. These findings reveal that the antioxidant and anti‐apoptotic characteristics of LS are acceptable defender pointers for the renal injury especially during gestational exposure to DNPs and/or FNT.

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Role of selenium and vitamin C in mitigating oxidative stress induced by fenitrothion in rat liver

Cited by 36 publications

References 42 publications

8:2 Fluorotelomer alcohol causes immunotoxicity and liver injury in adult male C57BL/6 mice

8:2 Fluorotelomer alcohol causes immunotoxicity and liver injury in adult male C57BL/6 mice

RETRACTED: Amorphous Selenium Nanoparticles Improve Vascular Function in Rats With Chronic Isocarbophos Poisoning via Inhibiting the Apoptosis of Vascular Endothelial Cells

Linseed ameliorates renal apoptosis in rat fetuses induced by single or combined exposure to diesel nanoparticles or fenitrothion by inhibiting transcriptional activation of p21/p53 and caspase‐3/9 through pro‐oxidant stimulus

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