Integrative proteomics and metabolomics analysis of non‐observable acute effect level PM2.5 induced accumulative effects in AC16 cells
Chronic exposure to very low ambient PM2.5 has been linked to cardiovascular risks in epidemiological observation, which also brought doubts on its safety threshold. In this study, we approached this question by chronic exposure of AC16 to the non‐observable acute effect level (NOAEL) PM2.5 5 μg/mL...
Gespeichert in:
Veröffentlicht in: | Journal of applied toxicology 2023-11, Vol.43 (11), p.1613-1629 |
---|---|
Hauptverfasser: | , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 1629 |
---|---|
container_issue | 11 |
container_start_page | 1613 |
container_title | Journal of applied toxicology |
container_volume | 43 |
creator | Bingru Nan Sun, Xia Yang, Shijing Huang, Qingyu Shen, Heqing |
description | Chronic exposure to very low ambient PM2.5 has been linked to cardiovascular risks in epidemiological observation, which also brought doubts on its safety threshold. In this study, we approached this question by chronic exposure of AC16 to the non‐observable acute effect level (NOAEL) PM2.5 5 μg/mL and its positive reference 50 μg/mL, respectively. The doses were respectively defined on the cell viabilities >95% (p = 0.354) and >90% (p = 0.004) when treated acutely (24 h). To mimic the long‐term exposure, AC16 was cultured from the 1st to 30th generations and treated with PM2.5 24 h in every three generations. The integration of proteomic and metabolomic analysis was applied, and 212 proteins and 172 metabolites were significantly altered during the experiments. The NOAEL PM2.5 induced both dose‐ and time‐dependent disruption, which showed the dynamic cellular proteomic response and oxidation accumulation, the main metabolomics changes were ribonucleotide, amino acid, and lipid metabolism that have involved in stressed gene expression, and starving for energy metabolism and lipid oxidation. In summary, these pathways interacted with the monotonically increasing oxidative stress and led to the accumulated damage in AC16 and implied that the safe threshold of PM2.5 may be non‐existent when a long‐term exposure occurred. |
doi_str_mv | 10.1002/jat.4500 |
format | Article |
fullrecord | <record><control><sourceid>proquest</sourceid><recordid>TN_cdi_proquest_miscellaneous_2823043626</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2823043626</sourcerecordid><originalsourceid>FETCH-LOGICAL-p216t-d47b55e4e2d1a9233f8747df2045ff2a3beccb7216a8105bd5d00741deb49a763</originalsourceid><addsrcrecordid>eNpd0DtLA0EQAOBFFIxR8Ccs2Nhc3OftXRmCj0BECwW7sI9ZubB3G7N7ATtLS3-jv8QL0cZqYOZjXgidUzKhhLCrlc4TIQk5QCNK6rqgrOSHaERYSQrB1csxOklpRchQY9UIfc67DK8bnZst4PUmZohtYxPWncMtZG1i-Evo8J6ahKPHXey-P76iSbDZahMAa9tnwOA92IwDbCHgx3s2kbjpXG_BDcD2bR_2Y_YuDUU8ndESWwghnaIjr0OCs984Rs8310-zu2LxcDufTRfFmtEyF04oIyUIYI7qmnHuKyWU84wI6T3T3IC1Rg1WV5RI46QjRAnqwIhaq5KP0eW-73DsWw8pL9sm7TbQHcQ-LVnFOBG8ZDt68Y-uYr8Z_rBTSrFKSlnzH2ixczs</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2877285559</pqid></control><display><type>article</type><title>Integrative proteomics and metabolomics analysis of non‐observable acute effect level PM2.5 induced accumulative effects in AC16 cells</title><source>Wiley-Blackwell Full Collection</source><creator>Bingru Nan ; Sun, Xia ; Yang, Shijing ; Huang, Qingyu ; Shen, Heqing</creator><creatorcontrib>Bingru Nan ; Sun, Xia ; Yang, Shijing ; Huang, Qingyu ; Shen, Heqing</creatorcontrib><description>Chronic exposure to very low ambient PM2.5 has been linked to cardiovascular risks in epidemiological observation, which also brought doubts on its safety threshold. In this study, we approached this question by chronic exposure of AC16 to the non‐observable acute effect level (NOAEL) PM2.5 5 μg/mL and its positive reference 50 μg/mL, respectively. The doses were respectively defined on the cell viabilities >95% (p = 0.354) and >90% (p = 0.004) when treated acutely (24 h). To mimic the long‐term exposure, AC16 was cultured from the 1st to 30th generations and treated with PM2.5 24 h in every three generations. The integration of proteomic and metabolomic analysis was applied, and 212 proteins and 172 metabolites were significantly altered during the experiments. The NOAEL PM2.5 induced both dose‐ and time‐dependent disruption, which showed the dynamic cellular proteomic response and oxidation accumulation, the main metabolomics changes were ribonucleotide, amino acid, and lipid metabolism that have involved in stressed gene expression, and starving for energy metabolism and lipid oxidation. In summary, these pathways interacted with the monotonically increasing oxidative stress and led to the accumulated damage in AC16 and implied that the safe threshold of PM2.5 may be non‐existent when a long‐term exposure occurred.</description><identifier>ISSN: 0260-437X</identifier><identifier>EISSN: 1099-1263</identifier><identifier>DOI: 10.1002/jat.4500</identifier><language>eng</language><publisher>Bognor Regis: Wiley Subscription Services, Inc</publisher><subject>Amino acid sequence ; Amino acids ; Chronic exposure ; Damage accumulation ; Energy metabolism ; Epidemiology ; Exposure ; Gene expression ; Health risks ; Lipid metabolism ; Lipid peroxidation ; Lipids ; Metabolism ; Metabolites ; Metabolomics ; Oxidation ; Oxidative stress ; Particulate matter ; Proteomics</subject><ispartof>Journal of applied toxicology, 2023-11, Vol.43 (11), p.1613-1629</ispartof><rights>2023 John Wiley & Sons, Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>Bingru Nan</creatorcontrib><creatorcontrib>Sun, Xia</creatorcontrib><creatorcontrib>Yang, Shijing</creatorcontrib><creatorcontrib>Huang, Qingyu</creatorcontrib><creatorcontrib>Shen, Heqing</creatorcontrib><title>Integrative proteomics and metabolomics analysis of non‐observable acute effect level PM2.5 induced accumulative effects in AC16 cells</title><title>Journal of applied toxicology</title><description>Chronic exposure to very low ambient PM2.5 has been linked to cardiovascular risks in epidemiological observation, which also brought doubts on its safety threshold. In this study, we approached this question by chronic exposure of AC16 to the non‐observable acute effect level (NOAEL) PM2.5 5 μg/mL and its positive reference 50 μg/mL, respectively. The doses were respectively defined on the cell viabilities >95% (p = 0.354) and >90% (p = 0.004) when treated acutely (24 h). To mimic the long‐term exposure, AC16 was cultured from the 1st to 30th generations and treated with PM2.5 24 h in every three generations. The integration of proteomic and metabolomic analysis was applied, and 212 proteins and 172 metabolites were significantly altered during the experiments. The NOAEL PM2.5 induced both dose‐ and time‐dependent disruption, which showed the dynamic cellular proteomic response and oxidation accumulation, the main metabolomics changes were ribonucleotide, amino acid, and lipid metabolism that have involved in stressed gene expression, and starving for energy metabolism and lipid oxidation. In summary, these pathways interacted with the monotonically increasing oxidative stress and led to the accumulated damage in AC16 and implied that the safe threshold of PM2.5 may be non‐existent when a long‐term exposure occurred.</description><subject>Amino acid sequence</subject><subject>Amino acids</subject><subject>Chronic exposure</subject><subject>Damage accumulation</subject><subject>Energy metabolism</subject><subject>Epidemiology</subject><subject>Exposure</subject><subject>Gene expression</subject><subject>Health risks</subject><subject>Lipid metabolism</subject><subject>Lipid peroxidation</subject><subject>Lipids</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Metabolomics</subject><subject>Oxidation</subject><subject>Oxidative stress</subject><subject>Particulate matter</subject><subject>Proteomics</subject><issn>0260-437X</issn><issn>1099-1263</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNpd0DtLA0EQAOBFFIxR8Ccs2Nhc3OftXRmCj0BECwW7sI9ZubB3G7N7ATtLS3-jv8QL0cZqYOZjXgidUzKhhLCrlc4TIQk5QCNK6rqgrOSHaERYSQrB1csxOklpRchQY9UIfc67DK8bnZst4PUmZohtYxPWncMtZG1i-Evo8J6ahKPHXey-P76iSbDZahMAa9tnwOA92IwDbCHgx3s2kbjpXG_BDcD2bR_2Y_YuDUU8ndESWwghnaIjr0OCs984Rs8310-zu2LxcDufTRfFmtEyF04oIyUIYI7qmnHuKyWU84wI6T3T3IC1Rg1WV5RI46QjRAnqwIhaq5KP0eW-73DsWw8pL9sm7TbQHcQ-LVnFOBG8ZDt68Y-uYr8Z_rBTSrFKSlnzH2ixczs</recordid><startdate>20231101</startdate><enddate>20231101</enddate><creator>Bingru Nan</creator><creator>Sun, Xia</creator><creator>Yang, Shijing</creator><creator>Huang, Qingyu</creator><creator>Shen, Heqing</creator><general>Wiley Subscription Services, Inc</general><scope>7ST</scope><scope>7TK</scope><scope>7U7</scope><scope>C1K</scope><scope>K9.</scope><scope>SOI</scope><scope>7X8</scope></search><sort><creationdate>20231101</creationdate><title>Integrative proteomics and metabolomics analysis of non‐observable acute effect level PM2.5 induced accumulative effects in AC16 cells</title><author>Bingru Nan ; Sun, Xia ; Yang, Shijing ; Huang, Qingyu ; Shen, Heqing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p216t-d47b55e4e2d1a9233f8747df2045ff2a3beccb7216a8105bd5d00741deb49a763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Amino acid sequence</topic><topic>Amino acids</topic><topic>Chronic exposure</topic><topic>Damage accumulation</topic><topic>Energy metabolism</topic><topic>Epidemiology</topic><topic>Exposure</topic><topic>Gene expression</topic><topic>Health risks</topic><topic>Lipid metabolism</topic><topic>Lipid peroxidation</topic><topic>Lipids</topic><topic>Metabolism</topic><topic>Metabolites</topic><topic>Metabolomics</topic><topic>Oxidation</topic><topic>Oxidative stress</topic><topic>Particulate matter</topic><topic>Proteomics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bingru Nan</creatorcontrib><creatorcontrib>Sun, Xia</creatorcontrib><creatorcontrib>Yang, Shijing</creatorcontrib><creatorcontrib>Huang, Qingyu</creatorcontrib><creatorcontrib>Shen, Heqing</creatorcontrib><collection>Environment Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Environment Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of applied toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bingru Nan</au><au>Sun, Xia</au><au>Yang, Shijing</au><au>Huang, Qingyu</au><au>Shen, Heqing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Integrative proteomics and metabolomics analysis of non‐observable acute effect level PM2.5 induced accumulative effects in AC16 cells</atitle><jtitle>Journal of applied toxicology</jtitle><date>2023-11-01</date><risdate>2023</risdate><volume>43</volume><issue>11</issue><spage>1613</spage><epage>1629</epage><pages>1613-1629</pages><issn>0260-437X</issn><eissn>1099-1263</eissn><abstract>Chronic exposure to very low ambient PM2.5 has been linked to cardiovascular risks in epidemiological observation, which also brought doubts on its safety threshold. In this study, we approached this question by chronic exposure of AC16 to the non‐observable acute effect level (NOAEL) PM2.5 5 μg/mL and its positive reference 50 μg/mL, respectively. The doses were respectively defined on the cell viabilities >95% (p = 0.354) and >90% (p = 0.004) when treated acutely (24 h). To mimic the long‐term exposure, AC16 was cultured from the 1st to 30th generations and treated with PM2.5 24 h in every three generations. The integration of proteomic and metabolomic analysis was applied, and 212 proteins and 172 metabolites were significantly altered during the experiments. The NOAEL PM2.5 induced both dose‐ and time‐dependent disruption, which showed the dynamic cellular proteomic response and oxidation accumulation, the main metabolomics changes were ribonucleotide, amino acid, and lipid metabolism that have involved in stressed gene expression, and starving for energy metabolism and lipid oxidation. In summary, these pathways interacted with the monotonically increasing oxidative stress and led to the accumulated damage in AC16 and implied that the safe threshold of PM2.5 may be non‐existent when a long‐term exposure occurred.</abstract><cop>Bognor Regis</cop><pub>Wiley Subscription Services, Inc</pub><doi>10.1002/jat.4500</doi><tpages>17</tpages></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0260-437X |
ispartof | Journal of applied toxicology, 2023-11, Vol.43 (11), p.1613-1629 |
issn | 0260-437X 1099-1263 |
language | eng |
recordid | cdi_proquest_miscellaneous_2823043626 |
source | Wiley-Blackwell Full Collection |
subjects | Amino acid sequence Amino acids Chronic exposure Damage accumulation Energy metabolism Epidemiology Exposure Gene expression Health risks Lipid metabolism Lipid peroxidation Lipids Metabolism Metabolites Metabolomics Oxidation Oxidative stress Particulate matter Proteomics |
title | Integrative proteomics and metabolomics analysis of non‐observable acute effect level PM2.5 induced accumulative effects in AC16 cells |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-25T05%3A32%3A32IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Integrative%20proteomics%20and%20metabolomics%20analysis%20of%20non%E2%80%90observable%20acute%20effect%20level%20PM2.5%20induced%20accumulative%20effects%20in%20AC16%20cells&rft.jtitle=Journal%20of%20applied%20toxicology&rft.au=Bingru%20Nan&rft.date=2023-11-01&rft.volume=43&rft.issue=11&rft.spage=1613&rft.epage=1629&rft.pages=1613-1629&rft.issn=0260-437X&rft.eissn=1099-1263&rft_id=info:doi/10.1002/jat.4500&rft_dat=%3Cproquest%3E2823043626%3C/proquest%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2877285559&rft_id=info:pmid/&rfr_iscdi=true |