Determination of Perflourooctanoic Acid Toxicity in a Human Hepatocarcinoma Cell Line.

IF 2.4 Q1 Medicine

Journal of Health and Pollution Pub Date : 2021-08-17 eCollection Date: 2021-09-01 DOI:10.5696/2156-9614-11.31.210909

Mahmoud Abudayyak, Ezgi Öztaş, Gül Özhan

{"title":"Determination of Perflourooctanoic Acid Toxicity in a Human Hepatocarcinoma Cell Line.","authors":"Mahmoud Abudayyak, Ezgi Öztaş, Gül Özhan","doi":"10.5696/2156-9614-11.31.210909","DOIUrl":null,"url":null,"abstract":"Background: Perfluorooctanoic acid (PFOA) is used in different industrial and commercial products. Research shows the presence of PFOA in home dusts, tap and surface water, and in biological samples. The International Agency for Research on Cancer (IARC) has classified PFOA as a possible carcinogen for humans. The liver is thought to be a target organ of PFOA accumulation and toxicity.Objective: Some studies have found toxic effects on the liver and related mechanisms; however, more studies are needed to better understand PFOA - induced hepatotoxicity.Methods: In the present study, a human hepatocarcinoma cell line was exposed to PFOA for 24 hours and cell viability, apoptosis, the oxidative system and immune response were evaluated.Results: While apoptosis was the main cell death pathway at low concentration (86.5%), the necrotic cell fraction increased with higher concentrations (46.7%). Significant changes in the reactive oxygen species (5.3-folds) glutathione (GSH) (1.7-folds) and catalase (CAT) (1.4-folds) levels were observed, as well as changes to interleukin-6 (≤1.8-fold) and interleukin-8 levels (35-40%).Conclusions: In light of the data, PFOA is potentially hepatotoxic through the investigated pathways. The results represent a background for future in vivo mechanistic studies.Competing interests: The authors declare no competing financial interests.","PeriodicalId":52138,"journal":{"name":"Journal of Health and Pollution","volume":" ","pages":"210909"},"PeriodicalIF":2.4000,"publicationDate":"2021-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8383792/pdf/","citationCount":"4","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Health and Pollution","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5696/2156-9614-11.31.210909","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2021/9/1 0:00:00","PubModel":"eCollection","JCR":"Q1","JCRName":"Medicine","Score":null,"Total":0}

引用次数: 4

Abstract

Background: Perfluorooctanoic acid (PFOA) is used in different industrial and commercial products. Research shows the presence of PFOA in home dusts, tap and surface water, and in biological samples. The International Agency for Research on Cancer (IARC) has classified PFOA as a possible carcinogen for humans. The liver is thought to be a target organ of PFOA accumulation and toxicity.

Objective: Some studies have found toxic effects on the liver and related mechanisms; however, more studies are needed to better understand PFOA - induced hepatotoxicity.

Methods: In the present study, a human hepatocarcinoma cell line was exposed to PFOA for 24 hours and cell viability, apoptosis, the oxidative system and immune response were evaluated.

Results: While apoptosis was the main cell death pathway at low concentration (86.5%), the necrotic cell fraction increased with higher concentrations (46.7%). Significant changes in the reactive oxygen species (5.3-folds) glutathione (GSH) (1.7-folds) and catalase (CAT) (1.4-folds) levels were observed, as well as changes to interleukin-6 (≤1.8-fold) and interleukin-8 levels (35-40%).

Conclusions: In light of the data, PFOA is potentially hepatotoxic through the investigated pathways. The results represent a background for future in vivo mechanistic studies.

Competing interests: The authors declare no competing financial interests.

Abstract Image

查看原文本刊更多论文

全氟辛酸对人肝癌细胞毒性的测定。

背景:全氟辛酸(PFOA)用于不同的工业和商业产品。研究表明，家庭灰尘、自来水和地表水以及生物样本中都存在全氟辛酸。国际癌症研究机构(IARC)已将全氟辛烷磺酸列为可能的人类致癌物。肝脏被认为是PFOA积累和毒性的靶器官。目的:一些研究发现了其对肝脏的毒性作用及其机制;然而，需要更多的研究来更好地了解PFOA引起的肝毒性。方法:将人肝癌细胞株暴露于PFOA作用24小时，观察细胞活力、凋亡、氧化系统和免疫反应。结果:低浓度时细胞凋亡是细胞死亡的主要途径(86.5%)，高浓度时坏死细胞比例增加(46.7%)。活性氧(5.3倍)、谷胱甘肽(1.7倍)、过氧化氢酶(1.4倍)水平及白细胞介素-6(≤1.8倍)、白细胞介素-8(35-40%)水平变化显著。结论:根据这些数据，PFOA通过所研究的途径具有潜在的肝毒性。该结果为未来的体内机制研究提供了背景。利益竞争:作者声明没有经济利益竞争。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Journal of Health and Pollution Medicine-Public Health, Environmental and Occupational Health

自引率

0.00%

发文量

审稿时长

18 weeks

期刊介绍： The Journal of Health and Pollution (JH&P) was initiated with funding from the European Union and World Bank and continues to be a Platinum Open Access Journal. There are no publication or viewing charges. That is, there are no charges to readers or authors. Upon peer-review and acceptance, all articles are made available online. The high-ranking editorial board is comprised of active members who participate in JH&P submissions and editorial policies. The Journal of Health and Pollution welcomes manuscripts based on original research as well as findings from re-interpretation and examination of existing data. JH&P focuses on point source pollution, related health impacts, environmental control and remediation technology. JH&P also has an interest in ambient and indoor pollution. Pollutants of particular interest include heavy metals, pesticides, radionuclides, dioxins, polychlorinated biphenyls (PCBs), polycyclic aromatic hydrocarbons (PAHs), volatile organic compounds (VOCs), air particulates (PM10 and PM2.5), and other severe and persistent toxins. JH&P emphasizes work relating directly to low and middle-income countries, however relevant work relating to high-income countries will be considered on a case-by-case basis.