Perfluorooctane sulfonate induces heart toxicity involving cardiac apoptosis and inflammation in rats

Xu, Dongyu; Li, Li; Tang, Leilei; Guo, Ming; Yang, Jie

doi:10.3892/etm.2021.10936

Cited by 15 publications

(20 citation statements)

References 39 publications

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Section: Discussionmentioning

confidence: 99%

“…Many in vivo and in vitro experiments have demonstrated that dysregulation of cytokine caused by environmental pollutants induces the inflammatory response 11 , 36 , 37 . For example, 10 mg/kg PFOS exposure was positively associated with the expression levels of IL-1β and TNF-α in rats after 14-day exposure 36 . PFAS can also induce a markable upregulation of proinflammatory cytokines TNF-α expression in the jejunum of the PFOS 1 mg/kg and 10 mg/kg groups compared with the control in rats 37 .…”

Section: Discussionmentioning

confidence: 99%

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Emerging and legacy PFAS and cytokine homeostasis in women of childbearing age

Nian

Zhou

Feng

et al. 2022

Sci Rep

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Per- and polyfluoroalkyl substances (PFAS) are widespread chemicals. Legacy PFAS have been phased out of production in most developed countries and emerging PFAS (short-chain PFAS and polyfluorinated compounds) are used as legacy PFAS alternatives. The effect of legacy and emerging PFAS on cytokine homeostasis in human remains poorly understood. This study aimed to evaluate the associations between legacy and emerging PFAS and cytokine profiles, and identify the main contributors to the disturbance of cytokine homeostasis. We quantified 21 PFAS in 198 Chinese women of childbearing age from 2015 to 2016. 13 cytokines were measured using the Meso Scale Discovery U-PLEX and V-PLEX platforms. The associations between PFAS exposure and cytokine levels were assessed using multiple linear regression (single-exposure), and Bayesian kernel machine regression (BKMR) models (PFAS mixture exposure). In single PFAS models, legacy and alternative PFAS were positively associated with Th1 and Treg cytokines, and negatively associated with Th2 and Th17 cytokines. For instance, each ln-unit increase in 6:2 chlorinated perfluoroalkyl ether sulfonic acid (6:2 Cl-PFESA), perfluorooctanoic acid (PFOA), and perfluorooctane sulfonate (PFOS) was associated with a decrease in IL-10 by − 0.228 (95% CI: − 0.336, − 0.120), − 0.153 (95% CI: − 0.277, − 0.030), and − 0.174 (95% CI: − 0.339, − 0.010), respectively. The BKMR model showed a significantly positive association of PFAS mixture with TGF-β and a negative association with IL-10. Overall, these results indicate that both legacy and emerging PFAS may affect the homeostasis of cytokines.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Emerging and legacy PFAS and cytokine homeostasis in women of childbearing age

Nian

Zhou

Feng

et al. 2022

Sci Rep

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“…12−15 For example, in Sprague-Dawley rats, PFOS induces cardiomyocyte apoptosis and inflammation, leading to the development of myocardial hypertrophy and fibrosis. 15 It is important to identify suitable medical agents, drug candidates, or antagonists to overcome the problem of PFOS exposure causing cardiac injury. CBD is considered a nonpsychoactive ingredient of cannabis without potential adverse cardiotoxicity.…”

Section: Discussionmentioning

confidence: 99%

“…12−14 Additionally, Xu et al showed that exposure of rats to PFOS induced an increase in heart weight/ body weight percentage, upregulation of P53, and Bax protein expression and cardiomyocyte apoptosis. 15 At present, although a few studies have reported the effect of PFOS on heart injury in rodents, the underlying molecular mechanism of PFOS-induced cardiac injury in mice is still unclear and needs to be further studied.…”

Section: Introductionmentioning

confidence: 99%

“…PFOS can also induce apoptosis of spleen and thymocytes by inducing ROS production and dissipation of mitochondrial membrane potential (MMP) . The heart is one of the main target organs of PFOS, and PFOS exposure has been found to result in mitochondrial damage and apoptosis of fetal myocardial cells. − Additionally, Xu et al showed that exposure of rats to PFOS induced an increase in heart weight/body weight percentage, upregulation of P53, and Bax protein expression and cardiomyocyte apoptosis . At present, although a few studies have reported the effect of PFOS on heart injury in rodents, the underlying molecular mechanism of PFOS-induced cardiac injury in mice is still unclear and needs to be further studied.…”

Section: Introductionmentioning

confidence: 99%

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Cannabidiol Alleviates Perfluorooctanesulfonic Acid-Induced Cardiomyocyte Apoptosis by Maintaining Mitochondrial Dynamic Balance and Energy Metabolic Homeostasis

Wang

Luo

et al. 2023

J. Agric. Food Chem.

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Perfluorooctanesulfonic acid (PFOS), a fluorine-containing organic compound, can be widely detected in the environment and living organisms. Accumulating evidence has shown that PFOS breaks through different biological barriers resulting in cardiac toxicity, but the underlying molecular mechanisms remain unclear. Cannabidiol (CBD) is a nonpsychoactive cannabinoid without potential adverse cardiotoxicity and has antioxidant and anti-inflammatory properties that reduce multiorgan damage and dysfunction. For these reasons, the aim of this study was to research how PFOS caused heart injury and whether CBD could attenuate PFOS-induced heart injury. Mice were fed PFOS (5 mg/kg) and/or CBD (10 mg/kg) in vivo. In vitro, H9C2 cells were intervened with PFOS (200 μM) and/or CBD (10 μM). After PFOS exposure, oxidative stress levels and the mRNA and protein expression of apoptosis-related markers increased distinctly, accompanied by mitochondrial dynamic imbalance and energy metabolism disorders in mouse heart and H9C2 cells. Moreover, terminal deoxynucleotidyl transferase dUTP nick end labeling staining, acridine orange/ethidium bromide staining and Hoechst 33258 staining signaled that the number of apoptotic cells increased after exposure to PFOS. Noteworthy, CBD simultaneous treatment alleviated a series of damages caused by PFOS-mediated oxidative stress. Our results demonstrated that CBD could alleviate PFOS-induced mitochondrial dynamics imbalance and energy metabolism disorder causing cardiomyocyte apoptosis by improving the antioxidant capacity, suggesting that CBD may represent a novel cardioprotective strategy against PFOS-induced cardiotoxicity. Our findings facilitate the understanding of the cardiotoxic effects of PFOS and the important role of CBD in protecting cardiac health.

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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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Perfluorooctane sulfonate induces heart toxicity involving cardiac apoptosis and inflammation in rats

Cited by 15 publications

References 39 publications

Emerging and legacy PFAS and cytokine homeostasis in women of childbearing age

Emerging and legacy PFAS and cytokine homeostasis in women of childbearing age

Cannabidiol Alleviates Perfluorooctanesulfonic Acid-Induced Cardiomyocyte Apoptosis by Maintaining Mitochondrial Dynamic Balance and Energy Metabolic Homeostasis

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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