Nikita David, Emma Ivantsova, Isaac Konig, Cole D English, Lev Avidan, Mark Kreychman, Mario L Rivera, Camilo Escobar, Eliana Maira Agostini Valle, Amany Sultan, Christopher J Martyniuk
{"title":"幼年斑马鱼(Danio rerio)暴露于全氟辛烷磺酰胺(PFOSA)后的不良后果:从神经毒性和行为角度看全氟辛烷磺酰胺。","authors":"Nikita David, Emma Ivantsova, Isaac Konig, Cole D English, Lev Avidan, Mark Kreychman, Mario L Rivera, Camilo Escobar, Eliana Maira Agostini Valle, Amany Sultan, Christopher J Martyniuk","doi":"10.3390/toxics12100723","DOIUrl":null,"url":null,"abstract":"<p><p>Toxicity mechanisms of per- and polyfluoroalkyl substances (PFASs), a chemical class present in diverse ecosystems, as well as many of their precursors, have been increasingly characterized in aquatic species. Perfluorooctanesulfonamide (PFOSA, C<sub>8</sub>H<sub>2</sub>F<sub>17</sub>NO<sub>2</sub>S) is a common precursor of perfluorooctane sulfonic acid (PFOS), a long-chain PFAS. Here, we assessed sub-lethal endpoints related to development, oxidative stress, transcript levels, and distance moved in zebrafish embryos and larvae following continuous exposure to PFOSA beginning at 6 h post-fertilization (hpf). PFOSA decreased survival in fish treated with 1 µg/L PFOSA; however, the effect was modest relative to the controls (difference of 10%). Exposure up to 10 µg/L PFOSA did not affect hatch rate, nor did it induce ROS in 7-day-old larvae fish. The activity of larval fish treated with 100 µg/L PFOSA was reduced relative to the solvent control. Transcripts related to oxidative stress response and apoptosis were measured and BCL2-associated X, apoptosis regulator (<i>bax</i>)<i>,</i> cytochrome c, somatic (<i>cycs</i>)<i>,</i> catalase (<i>cat</i>), superoxide dismutase 2 (<i>sod2</i>) were induced with high concentrations of PFOSA. Genes related to neurotoxicity were also measured and transcript levels of acetylcholinesterase (<i>ache</i>), elav-like RNA binding protein 3 (<i>elavl3</i>), growth-associated protein 43 (<i>gap43</i>), synapsin II (<i>syn2a</i>), and tubulin <i>3 (tubb3)</i> were all increased in larval fish with higher PFOSA exposure. These data improve our understanding of the potential sub-lethal toxicity of PFOSA in fish species.</p>","PeriodicalId":23195,"journal":{"name":"Toxics","volume":null,"pages":null},"PeriodicalIF":3.9000,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11510739/pdf/","citationCount":"0","resultStr":"{\"title\":\"Adverse Outcomes Following Exposure to Perfluorooctanesulfonamide (PFOSA) in Larval Zebrafish (<i>Danio rerio</i>): A Neurotoxic and Behavioral Perspective.\",\"authors\":\"Nikita David, Emma Ivantsova, Isaac Konig, Cole D English, Lev Avidan, Mark Kreychman, Mario L Rivera, Camilo Escobar, Eliana Maira Agostini Valle, Amany Sultan, Christopher J Martyniuk\",\"doi\":\"10.3390/toxics12100723\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Toxicity mechanisms of per- and polyfluoroalkyl substances (PFASs), a chemical class present in diverse ecosystems, as well as many of their precursors, have been increasingly characterized in aquatic species. Perfluorooctanesulfonamide (PFOSA, C<sub>8</sub>H<sub>2</sub>F<sub>17</sub>NO<sub>2</sub>S) is a common precursor of perfluorooctane sulfonic acid (PFOS), a long-chain PFAS. Here, we assessed sub-lethal endpoints related to development, oxidative stress, transcript levels, and distance moved in zebrafish embryos and larvae following continuous exposure to PFOSA beginning at 6 h post-fertilization (hpf). PFOSA decreased survival in fish treated with 1 µg/L PFOSA; however, the effect was modest relative to the controls (difference of 10%). Exposure up to 10 µg/L PFOSA did not affect hatch rate, nor did it induce ROS in 7-day-old larvae fish. The activity of larval fish treated with 100 µg/L PFOSA was reduced relative to the solvent control. Transcripts related to oxidative stress response and apoptosis were measured and BCL2-associated X, apoptosis regulator (<i>bax</i>)<i>,</i> cytochrome c, somatic (<i>cycs</i>)<i>,</i> catalase (<i>cat</i>), superoxide dismutase 2 (<i>sod2</i>) were induced with high concentrations of PFOSA. Genes related to neurotoxicity were also measured and transcript levels of acetylcholinesterase (<i>ache</i>), elav-like RNA binding protein 3 (<i>elavl3</i>), growth-associated protein 43 (<i>gap43</i>), synapsin II (<i>syn2a</i>), and tubulin <i>3 (tubb3)</i> were all increased in larval fish with higher PFOSA exposure. These data improve our understanding of the potential sub-lethal toxicity of PFOSA in fish species.</p>\",\"PeriodicalId\":23195,\"journal\":{\"name\":\"Toxics\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":3.9000,\"publicationDate\":\"2024-10-04\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11510739/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Toxics\",\"FirstCategoryId\":\"93\",\"ListUrlMain\":\"https://doi.org/10.3390/toxics12100723\",\"RegionNum\":3,\"RegionCategory\":\"环境科学与生态学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"ENVIRONMENTAL SCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Toxics","FirstCategoryId":"93","ListUrlMain":"https://doi.org/10.3390/toxics12100723","RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ENVIRONMENTAL SCIENCES","Score":null,"Total":0}
Adverse Outcomes Following Exposure to Perfluorooctanesulfonamide (PFOSA) in Larval Zebrafish (Danio rerio): A Neurotoxic and Behavioral Perspective.
Toxicity mechanisms of per- and polyfluoroalkyl substances (PFASs), a chemical class present in diverse ecosystems, as well as many of their precursors, have been increasingly characterized in aquatic species. Perfluorooctanesulfonamide (PFOSA, C8H2F17NO2S) is a common precursor of perfluorooctane sulfonic acid (PFOS), a long-chain PFAS. Here, we assessed sub-lethal endpoints related to development, oxidative stress, transcript levels, and distance moved in zebrafish embryos and larvae following continuous exposure to PFOSA beginning at 6 h post-fertilization (hpf). PFOSA decreased survival in fish treated with 1 µg/L PFOSA; however, the effect was modest relative to the controls (difference of 10%). Exposure up to 10 µg/L PFOSA did not affect hatch rate, nor did it induce ROS in 7-day-old larvae fish. The activity of larval fish treated with 100 µg/L PFOSA was reduced relative to the solvent control. Transcripts related to oxidative stress response and apoptosis were measured and BCL2-associated X, apoptosis regulator (bax), cytochrome c, somatic (cycs), catalase (cat), superoxide dismutase 2 (sod2) were induced with high concentrations of PFOSA. Genes related to neurotoxicity were also measured and transcript levels of acetylcholinesterase (ache), elav-like RNA binding protein 3 (elavl3), growth-associated protein 43 (gap43), synapsin II (syn2a), and tubulin 3 (tubb3) were all increased in larval fish with higher PFOSA exposure. These data improve our understanding of the potential sub-lethal toxicity of PFOSA in fish species.
ToxicsChemical Engineering-Chemical Health and Safety
CiteScore
4.50
自引率
10.90%
发文量
681
审稿时长
6 weeks
期刊介绍:
The Journal accepts papers describing work that furthers our understanding of the exposure, effects, and risks of chemicals and materials in humans and the natural environment as well as approaches to assess and/or manage the toxicological and ecotoxicological risks of chemicals and materials. The journal covers a wide range of toxic substances, including metals, pesticides, pharmaceuticals, biocides, nanomaterials, and polymers such as micro- and mesoplastics. Toxics accepts papers covering:
The occurrence, transport, and fate of chemicals and materials in different systems (e.g., food, air, water, soil);
Exposure of humans and the environment to toxic chemicals and materials as well as modelling and experimental approaches for characterizing the exposure in, e.g., water, air, soil, food, and consumer products;
Uptake, metabolism, and effects of chemicals and materials in a wide range of systems including in-vitro toxicological assays, aquatic and terrestrial organisms and ecosystems, model mammalian systems, and humans;
Approaches to assess the risks of chemicals and materials to humans and the environment;
Methodologies to eliminate or reduce the exposure of humans and the environment to toxic chemicals and materials.