Intestinal environmental disorders associate with the tissue damages induced by perfluorooctane sulfonate exposure

Wang, Gang; Sun, Shanshan; Wu, Xiaobing; Yang, Shurong; Wu, Yanmin; Zhao, Jianxin; Zhang, Hao; Chen, Wei

doi:10.1016/j.ecoenv.2020.110590

Cited by 66 publications

(32 citation statements)

References 45 publications

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“…There was a positive association between accumulative PFOA, another fluorocarbon, and the incidence of ulcerative colitis among 32,254 American adults (Steenland et al, 2013). Notably, previous research has focused on PFOS influence on gut microbiota and host metabolism (Wang et al, 2020;Zhang et al, 2020;Steenland et al, 2013;Steenland, Zhao & Winquist, 2015). Thus, information about PFOS in relation to pathological injury of small intestine in rodents is insufficient.…”

Section: Discussionmentioning

confidence: 99%

“…IBD is commonly characterized by transmural inflammation, especially neutrophil inflammation (Kelsen, Russo & Sullivan, 2019). Several studies have reported the inflammatory response caused by PFOS exposure (Wang et al, 2020;Gong et al, 2019). Wang et al (2020) have found that a short-term exposure to low doses of PFOS induced intestinal barrier damage, which led to peripheral inflammation that exacerbated liver injury in mice.…”

Section: Discussionmentioning

confidence: 99%

“…As a long half-life pollutant, PFOS can accumulate in the intestine, and improperly influence the enteral homeostasis under physiological and pathological conditions. C57BL/6J mice orally exposed to PFOS exhibited damaged microbiota and short-chain fatty acids, with modulated barrier function of the gut environment (Wang et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

“…For example, in vivo PFOS treatment induced atrophy of spleen and thymus (Qazi et al, 2009), and inhibited Th1 responses, while promoting Th2 responses (Zheng et al, 2009). PFOS treatment also caused hepatic metabolic dysfunction, which strongly correlated with alterations in microbiota composition (Zhang et al, 2020). As a long half-life pollutant, PFOS can accumulate in the intestine, and improperly influence the enteral homeostasis under physiological and pathological conditions.…”

Section: Introductionmentioning

confidence: 99%

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Perfluorooctane sulfonate exerts inflammatory bowel disease-like intestinal injury in rats

Hai

Yang

Zeng

et al. 2021

PeerJ

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Background Perfluorooctane sulfonate (PFOS), a type of perfluorinated compounds (PFCs), can induce various organ toxicity, including hepatomegaly, immunotoxicity, and gut microbiota disorder. PFCs have been associated with inflammatory bowel disease (IBD). Yet, whether PFOS exposure causes IBD-like disorder and the underlying mechanism remains undefined. Here, we investigated the influence of PFOS exposure on the development of IBD-like disorder in rats. Methods Sprague-Dawley rats were intraperitoneally injected with PFOS (1 or 10 mg/kg) or normal saline (NS) every other day for 15 days. Body weight, serum concentrations of serum amyloid A (SAA) and high sensitivity C reactive protein (hsCRP) were measured. Pathological assessments of villi height and crypt depth in the proximal duodenum and jejunum were performed using H&E staining. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining was used to assay cell apoptosis in the jejunum. The infiltration of inflammatory cells and cytokines in the jejunum were detected by immunohistochemistry analysis. Results PFOS (10 mg/kg) significantly increased the body weight, SAA and hsCRP, whereas no significant differences were observed in PFOS 1 mg/kg group of rats. The villi height and crypt depth in the proximal duodenum and jejunum were significantly reduced upon PFOS exposure. PFOS induced higher histopathological score in intestinal tissues compared to NS. Notably, TUNEL-positive cells were significantly higher in the jejunum upon PFOS exposure. Further, neutrophil and macrophage accumulated, and inflammatory cytokines infiltration were also remarkably increased in rats exposed to PFOS. Conclusion PFOS induces IBD-like phenotypes in rats, with associated inflammatory infiltration to intestinal.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Perfluorooctane sulfonate exerts inflammatory bowel disease-like intestinal injury in rats

Hai

Yang

Zeng

et al. 2021

PeerJ

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“…In addition, the network pharmacology analysis showed that the lipid metabolism-related pathway constituted potential protein targets of SFZYD [ 39 ]. The abundance of Ruminococcaceae and Prevotellaceae was increased significantly in SFZY rats relative to model rats, and these probiotics decompose complex carbohydrates into short-chain fatty acids (SCFAs) that are energy sources for intestinal epithelial cells and protective factors in gut inflammation [ 40 , 41 ]. As a consequence, SFZY would likely restore impaired gut microbiota and then promote SCFA production to improve the gut barrier, which would play a beneficial role in endometriosis treatment by reducing inflammation in the ectopic endometrium and in the pelvic cavity.…”

Section: Discussionmentioning

confidence: 99%

Letrozole and the Traditional Chinese Medicine, Shaofu Zhuyu Decoction, Reduce Endometriotic Disease Progression in Rats: A Potential Role for Gut Microbiota

Cao

Jiang

Jia

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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We previously showed that the Chinese herbal medicine, Shaofu Zhuyu decoction (SFZYD), shrank the size of endometriotic lesions in rats with endometriosis. We therefore conducted the present study to investigate the effects of letrozole and SFZYD on gut microbiota in endometriotic rats. Rats were divided into four groups: a blank group, model group, letrozole group, and SFZY group. Ectopic lesion size and COX-2 expression in the endometrium and endometriotic lesions were compared, and the community of gut microbiota was detected using 16S rRNA gene sequencing. Both letrozole and SFZYD reduced the size of ectopic lesions as well as lowered the expression of COX-2, thus reducing the inflammatory response. Compared with the blank group, the α-diversity of gut microbiota in endometriotic rats decreased, the Firmicutes/Bacteroidetes ratio increased, and the abundance of Ruminococcaceae was reduced. The α-diversity of gut microbiota in the letrozole group was similar to that in the model group, but the Firmicutes/Bacteroidetes ratio was diminished. The α-diversity in the SFZY group was similar to that in the blank group, the Firmicutes/Bacteroidetes ratio was attenuated, and the abundance of Ruminococcaceae was elevated compared with the model group. These results indicated that the therapeutic mechanisms of both letrozole and SFZYD were related to the restoration of gut microbiota.

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The therapeutic potential of isosakuranetin against perfluorooctane sulfonate instigated cardiac toxicity via modulating Nrf‐2/Keap‐1 pathway, inflammatory, apoptotic, and histological profile

Ijaz,

Shahid,

Hayat

et al. 2024

Cell Biochemistry & Function

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Perfluorooctane sulfonate (PFOS) is a pervasive organic toxicant that damages body organs, including heart. Isosakuranetin (ISN) is a plant‐based flavonoid that exhibits a broad range of pharmacological potentials. The current investigation was conducted to evaluate the potential role of ISN to counteract PFOS‐induced cardiac damage in rats. Twenty‐four albino rats (Rattus norvegicus) were distributed into four groups, including control, PFOS (10 mg/kg) intoxicated, PFOS + ISN (10 mg/kg + 20 mg/kg) treated, and ISN (20 mg/kg) alone supplemented group. It was revealed that PFOS intoxication reduced the expressions of Nrf‐2 and its antioxidant genes while escalating the expression of Keap‐1. Furthermore, PFOS exposure reduced the activities of glutathione reductase (GSR), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione S‐transferase (GST), Heme oxygenase‐1 (HO‐1) and glutathione (GSH) contents while upregulating the levels of reactive oxygen species (ROS) and malondialdehyde (MDA). Besides, PFOS administration upregulated the levels of creatine kinase‐MB (CK‐MB), troponin I, creatine phosphokinase (CPK), and lactate dehydrogenase (LDH). Moreover, the levels of tumor necrosis factor‐alpha (TNF‐α), nuclear factor kappa‐B (NF‐κB), interleukin‐6 (IL‐6), and interleukin‐1β (IL‐1β) were increased after PFOS intoxication. Additionally, PFOS exposure downregulated the expression of Bcl‐2 while upregulating the expressions of Bax and Caspase‐3. Furthermore, PFOS administration disrupted the normal architecture of cardiac tissues. Nonetheless, ISN treatment remarkably protected the cardiac tissues via regulating aforementioned dysregulations owing to its antioxidative, anti‐inflammatory, and antiapoptotic properties.

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Intestinal environmental disorders associate with the tissue damages induced by perfluorooctane sulfonate exposure

Cited by 66 publications

References 45 publications

Perfluorooctane sulfonate exerts inflammatory bowel disease-like intestinal injury in rats

Perfluorooctane sulfonate exerts inflammatory bowel disease-like intestinal injury in rats

Letrozole and the Traditional Chinese Medicine, Shaofu Zhuyu Decoction, Reduce Endometriotic Disease Progression in Rats: A Potential Role for Gut Microbiota

The therapeutic potential of isosakuranetin against perfluorooctane sulfonate instigated cardiac toxicity via modulating Nrf‐2/Keap‐1 pathway, inflammatory, apoptotic, and histological profile

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