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Ambient particulate matter exposure plus chronic ethanol ingestion exacerbates hepatic fibrosis by triggering the mitochondrial ROS-ferroptosis signaling pathway in mice
Chronic ethanol ingestion causes persistent oxidative stresses in the liver, leading to hepatic injury and fibrosis, but the underlying mechanisms remain unclear. Recently, ambient particulate matter (PM) has been confirmed to aggravate high-fat diet-induced liver fibrosis by enhancing oxidative str...
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Published in: | Ecotoxicology and environmental safety 2023-05, Vol.256, p.114897-114897, Article 114897 |
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description | Chronic ethanol ingestion causes persistent oxidative stresses in the liver, leading to hepatic injury and fibrosis, but the underlying mechanisms remain unclear. Recently, ambient particulate matter (PM) has been confirmed to aggravate high-fat diet-induced liver fibrosis by enhancing oxidative stress. Thus, we hypothesized that oxidative stress induced by ambient PM exposure increases the severity of liver fibrosis caused by ethanol ingestion.
C57BL/6 mice were subjected to ambient PM inhalation, ethanol ingestion or ambient PM-plus-ethanol ingestion for 12 weeks. Oxidative stress, mitochondrial reactive oxygen species (MtROS), liver fibrosis and ferroptosis indicators in the liver were evaluated. In vitro, oxidative stress, MtROS, ferroptosis indicators, profibrotic molecules and fibrosis markers in hepatic stellate (LX-2) cells were also determined. We found that ethanol ingestion markedly elevated hepatic oxidative stress and MtROS levels, triggered hepatic ferroptosis, and induced liver fibrosis, along with upregulation of the profibrotic molecule TGF-β1 and fibrosis marker collagen-I, in mice. Moreover, the combination of ambient PM and ethanol accelerated these adverse effects. Importantly, the combination of PM exposure and ethanol ingestion had a synergistic effect on these changes. In vitro, LX-2 cells activated with PM2.5 alone or combined with ethanol showed upregulation of TGF-β1 and collagen-I. In addition, the levels of MtROS, the oxidative stress marker 4-hydroxynonenal (4-HNE) and ferroptosis-related proteins and the GSH/GSSG ratio were significantly increased in PM2.5 plus ethanol-treated LX-2 cells. After pretreatment with a MtROS scavenger (Mito-TEMPO), we found that Mito-TEMPO treatment inhibited ferroptosis and oxidative stress in PM2.5 plus ethanol-treated LX-2 cells. Furthermore, a specific ferroptosis inhibitor (Fer-1) decreased the levels of ferroptosis-related proteins and profibrotic molecules in activated LX-2 cells co-exposed to PM2.5 and ethanol.
In this study, we revealed that ambient PM exposure induced profibrotic effects and that combined exposure to ambient PM and chronic ethanol ingestion exacerbated hepatic fibrosis, which may trigger ferroptosis by increasing MtROS, thereby activating hepatic stellate cells.
•Ambient particulate matter exposure plus chronic ethanol ingestion exacerbated liver fibrosis.•Ambient PM exposure activated the mitochondrial ROS-ferroptosis signaling pathway in liver.•Ambient PM plus ethanol in |
doi_str_mv | 10.1016/j.ecoenv.2023.114897 |
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C57BL/6 mice were subjected to ambient PM inhalation, ethanol ingestion or ambient PM-plus-ethanol ingestion for 12 weeks. Oxidative stress, mitochondrial reactive oxygen species (MtROS), liver fibrosis and ferroptosis indicators in the liver were evaluated. In vitro, oxidative stress, MtROS, ferroptosis indicators, profibrotic molecules and fibrosis markers in hepatic stellate (LX-2) cells were also determined. We found that ethanol ingestion markedly elevated hepatic oxidative stress and MtROS levels, triggered hepatic ferroptosis, and induced liver fibrosis, along with upregulation of the profibrotic molecule TGF-β1 and fibrosis marker collagen-I, in mice. Moreover, the combination of ambient PM and ethanol accelerated these adverse effects. Importantly, the combination of PM exposure and ethanol ingestion had a synergistic effect on these changes. In vitro, LX-2 cells activated with PM2.5 alone or combined with ethanol showed upregulation of TGF-β1 and collagen-I. In addition, the levels of MtROS, the oxidative stress marker 4-hydroxynonenal (4-HNE) and ferroptosis-related proteins and the GSH/GSSG ratio were significantly increased in PM2.5 plus ethanol-treated LX-2 cells. After pretreatment with a MtROS scavenger (Mito-TEMPO), we found that Mito-TEMPO treatment inhibited ferroptosis and oxidative stress in PM2.5 plus ethanol-treated LX-2 cells. Furthermore, a specific ferroptosis inhibitor (Fer-1) decreased the levels of ferroptosis-related proteins and profibrotic molecules in activated LX-2 cells co-exposed to PM2.5 and ethanol.
In this study, we revealed that ambient PM exposure induced profibrotic effects and that combined exposure to ambient PM and chronic ethanol ingestion exacerbated hepatic fibrosis, which may trigger ferroptosis by increasing MtROS, thereby activating hepatic stellate cells.
•Ambient particulate matter exposure plus chronic ethanol ingestion exacerbated liver fibrosis.•Ambient PM exposure activated the mitochondrial ROS-ferroptosis signaling pathway in liver.•Ambient PM plus ethanol ingestion exacerbated hepatic fibrosis via triggering mitochondrial ROS-ferroptosis pathway.</description><identifier>ISSN: 0147-6513</identifier><identifier>EISSN: 1090-2414</identifier><identifier>DOI: 10.1016/j.ecoenv.2023.114897</identifier><identifier>PMID: 37043943</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Animals ; Collagen Type I - adverse effects ; Eating ; Ethanol ; Ferroptosis ; Fibrosis ; Hepatic fibrosis ; Liver Cirrhosis - chemically induced ; Mice ; Mice, Inbred C57BL ; Mitochondrial reactive oxygen species ; Oxidative stress ; Particulate matter ; Particulate Matter - adverse effects ; Reactive Oxygen Species - metabolism ; Signal Transduction ; Transforming Growth Factor beta1</subject><ispartof>Ecotoxicology and environmental safety, 2023-05, Vol.256, p.114897-114897, Article 114897</ispartof><rights>2023 The Authors</rights><rights>Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-caeb845e1099f9436e1d7b5415515bd2c461b0457f0b00669fe4e43883d3d75e3</citedby><cites>FETCH-LOGICAL-c474t-caeb845e1099f9436e1d7b5415515bd2c461b0457f0b00669fe4e43883d3d75e3</cites><orcidid>0000-0001-9105-0385</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0147651323004013$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3549,27924,27925,45780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37043943$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ding, Shibin</creatorcontrib><creatorcontrib>Jiang, Jinjin</creatorcontrib><creatorcontrib>Zhang, Guofu</creatorcontrib><creatorcontrib>Yu, Min</creatorcontrib><creatorcontrib>Zheng, Yang</creatorcontrib><title>Ambient particulate matter exposure plus chronic ethanol ingestion exacerbates hepatic fibrosis by triggering the mitochondrial ROS-ferroptosis signaling pathway in mice</title><title>Ecotoxicology and environmental safety</title><addtitle>Ecotoxicol Environ Saf</addtitle><description>Chronic ethanol ingestion causes persistent oxidative stresses in the liver, leading to hepatic injury and fibrosis, but the underlying mechanisms remain unclear. Recently, ambient particulate matter (PM) has been confirmed to aggravate high-fat diet-induced liver fibrosis by enhancing oxidative stress. Thus, we hypothesized that oxidative stress induced by ambient PM exposure increases the severity of liver fibrosis caused by ethanol ingestion.
C57BL/6 mice were subjected to ambient PM inhalation, ethanol ingestion or ambient PM-plus-ethanol ingestion for 12 weeks. Oxidative stress, mitochondrial reactive oxygen species (MtROS), liver fibrosis and ferroptosis indicators in the liver were evaluated. In vitro, oxidative stress, MtROS, ferroptosis indicators, profibrotic molecules and fibrosis markers in hepatic stellate (LX-2) cells were also determined. We found that ethanol ingestion markedly elevated hepatic oxidative stress and MtROS levels, triggered hepatic ferroptosis, and induced liver fibrosis, along with upregulation of the profibrotic molecule TGF-β1 and fibrosis marker collagen-I, in mice. Moreover, the combination of ambient PM and ethanol accelerated these adverse effects. Importantly, the combination of PM exposure and ethanol ingestion had a synergistic effect on these changes. In vitro, LX-2 cells activated with PM2.5 alone or combined with ethanol showed upregulation of TGF-β1 and collagen-I. In addition, the levels of MtROS, the oxidative stress marker 4-hydroxynonenal (4-HNE) and ferroptosis-related proteins and the GSH/GSSG ratio were significantly increased in PM2.5 plus ethanol-treated LX-2 cells. After pretreatment with a MtROS scavenger (Mito-TEMPO), we found that Mito-TEMPO treatment inhibited ferroptosis and oxidative stress in PM2.5 plus ethanol-treated LX-2 cells. Furthermore, a specific ferroptosis inhibitor (Fer-1) decreased the levels of ferroptosis-related proteins and profibrotic molecules in activated LX-2 cells co-exposed to PM2.5 and ethanol.
In this study, we revealed that ambient PM exposure induced profibrotic effects and that combined exposure to ambient PM and chronic ethanol ingestion exacerbated hepatic fibrosis, which may trigger ferroptosis by increasing MtROS, thereby activating hepatic stellate cells.
•Ambient particulate matter exposure plus chronic ethanol ingestion exacerbated liver fibrosis.•Ambient PM exposure activated the mitochondrial ROS-ferroptosis signaling pathway in liver.•Ambient PM plus ethanol ingestion exacerbated hepatic fibrosis via triggering mitochondrial ROS-ferroptosis pathway.</description><subject>Animals</subject><subject>Collagen Type I - adverse effects</subject><subject>Eating</subject><subject>Ethanol</subject><subject>Ferroptosis</subject><subject>Fibrosis</subject><subject>Hepatic fibrosis</subject><subject>Liver Cirrhosis - chemically induced</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mitochondrial reactive oxygen species</subject><subject>Oxidative stress</subject><subject>Particulate matter</subject><subject>Particulate Matter - adverse effects</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Signal Transduction</subject><subject>Transforming Growth Factor beta1</subject><issn>0147-6513</issn><issn>1090-2414</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNp9kctu1DAYhS0EokPhDRDykk0GO3ZuG6Sq4lKpUiUua8t2_iQeJXGwnZZ5JN6SfyalS1aWrO-cY59DyFvO9pzx8sNhD9bDfL_PWS72nMu6qZ6RHWcNy3LJ5XOyY1xWWVlwcUFexXhgjAlWFC_JhaiYFI0UO_LnajIO5kQXHZKz66gT0EmnBIHC78XHNQBdxjVSOwQ_O0shDXr2I3VzDzE5PyOnLQSDykgHWDT60M6Z4KOL1BxpCq7vIaCApgHdXfJ28HMbnB7pt7vvWQch-CWd-ej6WY8nFo2GB33EIJRYeE1edHqM8ObxvCQ_P3_6cf01u737cnN9dZtZWcmUWQ2mlgVgD02HXyyBt5UpJC8KXpg2t7Lkhsmi6phhrCybDiRIUdeiFW1VgLgkN5tv6_VBLcFNOhyV106dL3zo1bmqEZToLNM1qzjkrZS6NDpnpcixXFZB3Wj0er95LcH_WrEuNbloYRz1DH6NKq_xCXmJIkTlhlrsLQbonqI5U6fB1UFtg6vT4GobHGXvHhNWM0H7JPq3MAIfNwCws3sHQUWLg1toXQCb8FPu_wl_Ac-ZwdA</recordid><startdate>202305</startdate><enddate>202305</enddate><creator>Ding, Shibin</creator><creator>Jiang, Jinjin</creator><creator>Zhang, Guofu</creator><creator>Yu, Min</creator><creator>Zheng, Yang</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0001-9105-0385</orcidid></search><sort><creationdate>202305</creationdate><title>Ambient particulate matter exposure plus chronic ethanol ingestion exacerbates hepatic fibrosis by triggering the mitochondrial ROS-ferroptosis signaling pathway in mice</title><author>Ding, Shibin ; Jiang, Jinjin ; Zhang, Guofu ; Yu, Min ; Zheng, Yang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-caeb845e1099f9436e1d7b5415515bd2c461b0457f0b00669fe4e43883d3d75e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Animals</topic><topic>Collagen Type I - adverse effects</topic><topic>Eating</topic><topic>Ethanol</topic><topic>Ferroptosis</topic><topic>Fibrosis</topic><topic>Hepatic fibrosis</topic><topic>Liver Cirrhosis - chemically induced</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mitochondrial reactive oxygen species</topic><topic>Oxidative stress</topic><topic>Particulate matter</topic><topic>Particulate Matter - adverse effects</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Signal Transduction</topic><topic>Transforming Growth Factor beta1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ding, Shibin</creatorcontrib><creatorcontrib>Jiang, Jinjin</creatorcontrib><creatorcontrib>Zhang, Guofu</creatorcontrib><creatorcontrib>Yu, Min</creatorcontrib><creatorcontrib>Zheng, Yang</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Directory of Open Access Journals</collection><jtitle>Ecotoxicology and environmental safety</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ding, Shibin</au><au>Jiang, Jinjin</au><au>Zhang, Guofu</au><au>Yu, Min</au><au>Zheng, Yang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ambient particulate matter exposure plus chronic ethanol ingestion exacerbates hepatic fibrosis by triggering the mitochondrial ROS-ferroptosis signaling pathway in mice</atitle><jtitle>Ecotoxicology and environmental safety</jtitle><addtitle>Ecotoxicol Environ Saf</addtitle><date>2023-05</date><risdate>2023</risdate><volume>256</volume><spage>114897</spage><epage>114897</epage><pages>114897-114897</pages><artnum>114897</artnum><issn>0147-6513</issn><eissn>1090-2414</eissn><abstract>Chronic ethanol ingestion causes persistent oxidative stresses in the liver, leading to hepatic injury and fibrosis, but the underlying mechanisms remain unclear. Recently, ambient particulate matter (PM) has been confirmed to aggravate high-fat diet-induced liver fibrosis by enhancing oxidative stress. Thus, we hypothesized that oxidative stress induced by ambient PM exposure increases the severity of liver fibrosis caused by ethanol ingestion.
C57BL/6 mice were subjected to ambient PM inhalation, ethanol ingestion or ambient PM-plus-ethanol ingestion for 12 weeks. Oxidative stress, mitochondrial reactive oxygen species (MtROS), liver fibrosis and ferroptosis indicators in the liver were evaluated. In vitro, oxidative stress, MtROS, ferroptosis indicators, profibrotic molecules and fibrosis markers in hepatic stellate (LX-2) cells were also determined. We found that ethanol ingestion markedly elevated hepatic oxidative stress and MtROS levels, triggered hepatic ferroptosis, and induced liver fibrosis, along with upregulation of the profibrotic molecule TGF-β1 and fibrosis marker collagen-I, in mice. Moreover, the combination of ambient PM and ethanol accelerated these adverse effects. Importantly, the combination of PM exposure and ethanol ingestion had a synergistic effect on these changes. In vitro, LX-2 cells activated with PM2.5 alone or combined with ethanol showed upregulation of TGF-β1 and collagen-I. In addition, the levels of MtROS, the oxidative stress marker 4-hydroxynonenal (4-HNE) and ferroptosis-related proteins and the GSH/GSSG ratio were significantly increased in PM2.5 plus ethanol-treated LX-2 cells. After pretreatment with a MtROS scavenger (Mito-TEMPO), we found that Mito-TEMPO treatment inhibited ferroptosis and oxidative stress in PM2.5 plus ethanol-treated LX-2 cells. Furthermore, a specific ferroptosis inhibitor (Fer-1) decreased the levels of ferroptosis-related proteins and profibrotic molecules in activated LX-2 cells co-exposed to PM2.5 and ethanol.
In this study, we revealed that ambient PM exposure induced profibrotic effects and that combined exposure to ambient PM and chronic ethanol ingestion exacerbated hepatic fibrosis, which may trigger ferroptosis by increasing MtROS, thereby activating hepatic stellate cells.
•Ambient particulate matter exposure plus chronic ethanol ingestion exacerbated liver fibrosis.•Ambient PM exposure activated the mitochondrial ROS-ferroptosis signaling pathway in liver.•Ambient PM plus ethanol ingestion exacerbated hepatic fibrosis via triggering mitochondrial ROS-ferroptosis pathway.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>37043943</pmid><doi>10.1016/j.ecoenv.2023.114897</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0001-9105-0385</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Animals Collagen Type I - adverse effects Eating Ethanol Ferroptosis Fibrosis Hepatic fibrosis Liver Cirrhosis - chemically induced Mice Mice, Inbred C57BL Mitochondrial reactive oxygen species Oxidative stress Particulate matter Particulate Matter - adverse effects Reactive Oxygen Species - metabolism Signal Transduction Transforming Growth Factor beta1 |
title | Ambient particulate matter exposure plus chronic ethanol ingestion exacerbates hepatic fibrosis by triggering the mitochondrial ROS-ferroptosis signaling pathway in mice |
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