<i>Cis</i>
-bifenthrin induces immunotoxicity in adolescent male C57BL/6 mice

Wang, Xia; Gao, Xingli; He, Bingnan; Zhu, Jiawei; Lou, Huihui; Hu, Qinglian; Jin, Yuanxiang; Fu, Zhengwei

doi:10.1002/tox.22407

Cited by 13 publications

(8 citation statements)

References 39 publications

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“…The results of our study are similar to the results obtained by Wang et al who conducted an experiment on male mice exposed to bifenthrin for 3 weeks and confirmed immunotoxic effect of the pyrethroid [25]. Another study published by Wang et al elucidated the mechanisms of bifenthrin's immunotoxicity in murine macrophages.…”

Section: Discussionsupporting

confidence: 92%

Subacute poisoning with bifenthrin increases the level of interleukin 1ß in mice kidneys and livers

Pylak-Piwko

Nieradko-Iwanicka

2021

BMC Pharmacol Toxicol

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Background Bifenthrin is a pyrethroid. Chronic exposure of humans to the pesticide occurs. Reports about immunotoxicity and proinflammatory effect of pyrethroids were published. The aim of the article was to check if subacute poisoning with bifenthrin affects proinflammatory interleukin 1ß and tumor necrosis factorα (TNFα) in kidneys, livers and the function of these organs. Methods Thirty two female mice were used. They were divided into 4 groups: controls, mice receiving 1.61 mg/kg bifenthrin for 28 days (group 1), 4.025 mg/kg (2), 8.05 mg/kg (3). On day 29 they were sacrificed, blood, livers and kidneys were obtained. Creatinine concentration and alanine transaminase (ALT) activity were estimated in the blood sera. Interleukin1ß and TNFα concentrations in the organs were measured. Result Mean interleukin 1ß concentration in the livers of controls was 53 pg/ml, in group 1- 54 pg/ml, 2- 59 pg/ml, 3- 99 pg/ml (p < 0.05 vs controls). It was accompanied by significant increase in ALT activity in group 3 vs controls (p < 0.05). In the control kidneys interleukin 1ß was 3.9 pg/ml, group 1–6.8 pg/ml, 2–9.8 pg/ml and 3- 11 pg/ml. Statistically significant difference between group 1, 2 and 3 vs controls was found. There was no significant differences among the groups in TNFα concentrations neither in the livers nor kidneys. Conclusion Subacute poisoning with bifenthrin significantly increases interleukin 1ß concentration in livers and kidneys in a dose-proportionate level. It is accompanied by ALT activity increase. It confirms nephrotoxic and hepatotoxic and pro-inflammatory effect of bifenthrin in non-target organisms.

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Section: Discussionsupporting

confidence: 92%

Subacute poisoning with bifenthrin increases the level of interleukin 1ß in mice kidneys and livers

Pylak-Piwko

Nieradko-Iwanicka

2021

BMC Pharmacol Toxicol

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“…A quintessential example is that ConA‐stimulated T cell proliferation in B6C3F1 female mouse splenocytes was inhibited by PFOS exposure . Our previous study demonstrated that the pesticide cis ‐bifenthrin inhibited the LPS‐ or ConA‐stimulated cell proliferation of primary cultured splenocytes . Consistent with these observations, the present study showed that 8:2 FTOH inhibited the splenocyte proliferation stimulated by ConA and LPS (Figure A,B), indicating that 8:2 FTOH inhibited both humoral and cellular immunity.…”

Section: Discussionsupporting

confidence: 89%

“…Dysfunction of the immune system can lead to autoimmune diseases, infections, and cancers . Until now, a number of studies have demonstrated that a wide range of xenobiotics can result in the disruption of immune function . FTOHs can be taken up via the breath and routine diet in mammals and then distributed through the bloodstream.…”

Section: Introductionmentioning

confidence: 99%

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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“…Intracellular ROS level is elevated by many xenobiotic substances, underlying the mechanism of caused cellular toxicity, including some PFASs . However, 6:2 FTOH and 8:2 FTOH did not cause oxidative DNA damage in rat testicular cells .…”

Section: Discussionmentioning

confidence: 94%

“…A broad range of industrial and environmental chemicals have been suggested to target immune system . It has been observed that the incidence of immune‐related diseases has been increasing throughout the recent decades, part of which can be traced back to an interference in immune function .…”

Section: Introductionmentioning

confidence: 99%

8:2 Fluorotelomer alcohol causes G1 cell cycle arrest and blocks granulocytic differentiation in HL‐60 cells

Wang

Zhou

et al. 2019

Environmental Toxicology

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Fluorotelomer alcohols (FTOHs) are fluorinated intermediates used in manufacturing specialty polymer and surfactants, with 8:2 FTOH the homologue of largest production. FTOHs were found to pose acute toxicity, hepatotoxicity, nephrotoxicity, developmental toxicity and endocrine-disrupting risks, whereas research regarding immunotoxicity and its underlying mechanism, especially on specific immune cells is limited. Here, we investigated the immunotoxicity of 8:2 FTOH on immature immune cells in an in vitro system. We observed that exposure of HL-60 cells, a human promyelocytic leukemic cell line, to 8:2 FTOH reduced cell viability in a dose-and time-dependent manner. In addition, 8:2 FTOH exposure caused G1 cell cycle arrest in HL-60 cells, while it showed no effect on apoptosis. Exposure to 8:2 FTOH inhibited the mRNA expression of cell cycle-related genes, including CCNA1, CCNA2, CCND1, and CCNE2. Moreover, exposure to 8:2 FTOH inhibited the mRNA expression of granulocytic differentiation-related genes of CD11b, CSF3R, PU.1, and C/EPBε in HL-60 cells . Furthermore, 8:2 FTOH exhibited no effect on intracellular ROS level, while hydralazine hydrochloride (Hyd), one reactive carbonyl species (RCS) scavenger, partially blocked 8:2 FTOH-caused cytotoxicity in HL-60 cells. Overall, the results obtained in the study show that 8:2 FTOH poses immunotoxicity in immature immune cells and RCS may partially underline its mechanism. K E Y W O R D S 8:2 FTOH, cell cycle arrest, differentiation block, immature immune cells, immunotoxicity, reactive carbonyl species

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Cis -bifenthrin induces immunotoxicity in adolescent male C57BL/6 mice

Cited by 13 publications

References 39 publications

Subacute poisoning with bifenthrin increases the level of interleukin 1ß in mice kidneys and livers

Subacute poisoning with bifenthrin increases the level of interleukin 1ß in mice kidneys and livers

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

8:2 Fluorotelomer alcohol causes G1 cell cycle arrest and blocks granulocytic differentiation in HL‐60 cells

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