The Role of Ferroptosis in the Damage of Human Proximal Tubule Epithelial Cells Caused by Perfluorooctane Sulfonate

Wang, Pingwei; Liu, Dongge; Yan, Shuqi; Liang, Yujun; Cui, Jiajing; Guo, Li; Ren, Shuping; Chen, Peng

doi:10.3390/toxics10080436

Cited by 7 publications

(3 citation statements)

References 58 publications

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“…Liver: hepatotoxic NAFLD, liver fibrosis, markers change [198,200,385,[386][387][388] 2. Kidney: nephrotoxic Reduced excretion of toxins [204,389,390]; increased incidence of CKD [203,391]; ferroptosis [392] 3. Lungs/bronchi Promotion of asthma in youth [393] 4.…”

Section: Affected Organ/function Consequencesmentioning

confidence: 99%

PFAS: forever chemicals—persistent, bioaccumulative and mobile. Reviewing the status and the need for their phase out and remediation of contaminated sites

Brunn

Arnold²,

Körner

et al. 2023

Environ Sci Eur

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Background Per- and polyfluorinated alkyl substances (PFAS) have received increasing scientific and political attention in recent years. Several thousand commercially produced compounds are used in numerous products and technical processes. Due to their extreme persistence in the environment, humans and all other life forms are, therefore, increasingly exposed to these substances. In the following review, PFAS will be examined comprehensively. Results The best studied PFAS are carboxylic and sulfonic acids with chain lengths of C4 to C14, particularly perfluorooctanoic acid (PFOA) and perfluorooctane sulfonic acid (PFOS). These substances are harmful to aquatic fauna, insects, and amphibians at concentrations of a few µg/L or less, accumulate in organisms, and biomagnify in food webs. Humans, as the final link in numerous food chains, are subjected to PFAS uptake primarily through food and drinking water. Several PFAS have multiple toxic effects, particularly affecting liver, kidney, thyroid, and the immune system. The latter effect is the basis for the establishment of a tolerable weekly dose of only 4.4 ng/kg body weight for the sum of the four representatives PFOA, PFOS, perfluorononanoic acid (PFNA) and perfluorohexane sulfonic acid (PFHxS) by the European Food Safety Authority (EFSA) in 2020. Exposure estimates and human biomonitoring show that this value is frequently reached, and in many cases exceeded. PFAS are a major challenge for analysis, especially of products and waste: single-substance analyses capture only a fragment of the large, diverse family of PFAS. As a consequence, sum parameters have gained increasing importance. The high mobility of per and polyfluorinated carboxylic and sulfonic acids makes soil and groundwater pollution at contaminated sites a problem. In general, short-chain PFAS are more mobile than long-chain ones. Processes for soil and groundwater purification and drinking water treatment are often ineffective and expensive. Recycling of PFAS-containing products such as paper and food packaging leads to carryover of the contaminants. Incineration requires high temperatures to completely destroy PFAS. After PFOA, PFOS and a few other perfluorinated carboxylic and sulfonic acids were regulated internationally, many manufacturers and users switched to other PFAS: short-chain representatives, per- and polyfluorinated oxo carboxylic acids, telomeric alcohols and acids. Analytical studies show an increase in environmental concentrations of these chemicals. Ultra-short PFAS (chain length C1–C3) have not been well studied. Among others, trifluoroacetic acid (TFA) is present globally in rapidly increasing concentrations. Conclusions The substitution of individual PFAS recognized as hazardous by other possibly equally hazardous PFAS with virtually unknown chronic toxicity can, therefore, not be a solution. The only answer is a switch to fluorine-free alternatives for all applications in which PFAS are not essential.

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Section: Affected Organ/function Consequencesmentioning

confidence: 99%

PFAS: forever chemicals—persistent, bioaccumulative and mobile. Reviewing the status and the need for their phase out and remediation of contaminated sites

Brunn

Arnold²,

Körner

et al. 2023

Environ Sci Eur

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“…The study further suggested the involvement of ferroptosis in PFAS-induced effects, indicating the potential role of this mechanism in the toxicological response to PFCs. Moreover, the role of ferroptosis was also examined in PFOS-induced endothelial dysfunction . PFOS exposure was found to cause a decrease in cell viability and morphological changes and increased lipid droplet accumulation in human umbilical vein endothelial cells (HUVECs).…”

Section: Ferroptosis Inducers In Environmental Pollutantsmentioning

confidence: 99%

“…Moreover, the role of ferroptosis was also examined in PFOS-induced endothelial dysfunction. 78 PFOS exposure was found to cause a decrease in cell viability and morphological changes and increased lipid droplet accumulation in human umbilical vein endothelial cells (HUVECs). Furthermore, PFOS downregulated the expression of GPX4 and ferritin heavy chain protein 1 (FTH1) while upregulating ACSL4.…”

Section: Perfluorochemicals (Pfcs)mentioning

confidence: 99%

Ferroptosis Induced by Pollutants: An Emerging Mechanism in Environmental Toxicology

Yang,

Cai,

2024

Environ. Sci. Technol.

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Environmental pollutants have been recognized for their ability to induce various adverse outcomes in both the environment and human health, including inflammation, apoptosis, necrosis, pyroptosis, and autophagy. Understanding these biological mechanisms has played a crucial role in risk assessment and management efforts. However, the recent identification of ferroptosis as a form of programmed cell death has emerged as a critical mechanism underlying pollutant-induced toxicity. Numerous studies have demonstrated that fine particulates, heavy metals, and organic substances can trigger ferroptosis, which is closely intertwined with lipid, iron, and amino acid metabolism. Given the growing evidence linking ferroptosis to severe diseases such as heart failure, chronic obstructive pulmonary disease, liver injury, Parkinson's disease, Alzheimer's disease, and cancer, it is imperative to investigate the role of pollutant-induced ferroptosis. In this review, we comprehensively analyze various pollutant-induced ferroptosis pathways and intricate signaling molecules and elucidate their integration into the driving and braking axes. Furthermore, we discuss the potential hazards associated with pollutant-induced ferroptosis in various organs and four representative animal models. Finally, we provide an outlook on future research directions and strategies aimed at preventing pollutant-induced ferroptosis. By enhancing our understanding of this novel form of cell death and developing effective preventive measures, we can mitigate the adverse effects of environmental pollutants and safeguard human and environmental health.

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Sodium aescinate induces renal toxicity by promoting Nrf2/GPX4-mediated ferroptosis

Zhu,

Duan,

Yang

et al. 2024

Chemico-Biological Interactions

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The Role of Ferroptosis in the Damage of Human Proximal Tubule Epithelial Cells Caused by Perfluorooctane Sulfonate

Cited by 7 publications

References 58 publications

PFAS: forever chemicals—persistent, bioaccumulative and mobile. Reviewing the status and the need for their phase out and remediation of contaminated sites

PFAS: forever chemicals—persistent, bioaccumulative and mobile. Reviewing the status and the need for their phase out and remediation of contaminated sites

Ferroptosis Induced by Pollutants: An Emerging Mechanism in Environmental Toxicology

Sodium aescinate induces renal toxicity by promoting Nrf2/GPX4-mediated ferroptosis

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