Kidney damage induced by repeated fine particulate matter exposure: Effects of different components
Exposure to fine particulate matter with an aerodynamic diameter of ≤2.5 μm (PM2.5) is associated with adverse health effects. This study aimed to evaluate the toxic effects of the constituents of PM2.5 on mouse kidneys. We collected PM2.5 near an industrial complex located in southern Kaohsiung, Ta...
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Veröffentlicht in: | The Science of the total environment 2022-11, Vol.847, p.157528-157528, Article 157528 |
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description | Exposure to fine particulate matter with an aerodynamic diameter of ≤2.5 μm (PM2.5) is associated with adverse health effects. This study aimed to evaluate the toxic effects of the constituents of PM2.5 on mouse kidneys.
We collected PM2.5 near an industrial complex located in southern Kaohsiung, Taiwan, that was divided into water extract and insoluble particles. Male C57BL/6 mice were divided into five groups: control, low- and high-dose insoluble particle exposure, and low- and high-dose water extract exposure. Biochemical analysis, Western blot analysis, histological examination, and immunohistochemistry were performed to evaluate the impact of PM2.5 constituents on mice kidneys.
PM2.5 was collected from January 1, 2021, to February 8, 2021, from an industrial complex in Kaohsiung, Taiwan. Metallic element analysis showed that Pb, Ni, V, and Ti were non-essential metals with enrichment factors >10. Polycyclic aromatic hydrocarbon and nitrate polycyclic aromatic hydrocarbon analyses revealed that the toxic equivalents are, in the order, benzo(a)pyrene (BaP), indeno(1,2,3-cd) pyrene (IP), dibenzo(a,h)anthracene (DBA), and benzo(b)fluoranthene (BbF), which are potential carcinogens. Both water extract and insoluble particle exposure induced inflammatory cytokine upregulation, inflammatory cell infiltration, antioxidant activity downregulation, and elevation of kidney injury molecule 1 (KIM-1) level in mouse kidneys. A dose-dependent effect of PM2.5 water extract and insoluble particle exposure on angiotensin converter enzyme 2 downregulation in mouse kidneys was observed.
We found that water-soluble extract and insoluble particles of PM2.5 could induce oxidative stress and inflammatory reactions, influence the regulation of renin-angiotensin system (RAS), and lead to kidney injury marker level elevation in mouse kidneys. The lowest-observed-adverse-effect level for renal toxicity in mice was 40 μg water-soluble extract/insoluble particle inhalation per week, which was approximately equal to the ambient PM2.5 concentration of 44 μg/m3 for mice.
[Display omitted]
•PM2.5 collected at the Kaohsiung industrial complex was chemically analyzed.•Water extracts and insoluble particles of PM2.5 induced inflammatory cell infiltration in mouse kidneys.•W PM2.5 induced angiotensin-converting enzyme 2 downregulation in mouse kidney.•PM2.5 induced antioxidant activity downregulation.•Water extracts and insoluble particle induced apoptosis expression. |
doi_str_mv | 10.1016/j.scitotenv.2022.157528 |
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We collected PM2.5 near an industrial complex located in southern Kaohsiung, Taiwan, that was divided into water extract and insoluble particles. Male C57BL/6 mice were divided into five groups: control, low- and high-dose insoluble particle exposure, and low- and high-dose water extract exposure. Biochemical analysis, Western blot analysis, histological examination, and immunohistochemistry were performed to evaluate the impact of PM2.5 constituents on mice kidneys.
PM2.5 was collected from January 1, 2021, to February 8, 2021, from an industrial complex in Kaohsiung, Taiwan. Metallic element analysis showed that Pb, Ni, V, and Ti were non-essential metals with enrichment factors >10. Polycyclic aromatic hydrocarbon and nitrate polycyclic aromatic hydrocarbon analyses revealed that the toxic equivalents are, in the order, benzo(a)pyrene (BaP), indeno(1,2,3-cd) pyrene (IP), dibenzo(a,h)anthracene (DBA), and benzo(b)fluoranthene (BbF), which are potential carcinogens. Both water extract and insoluble particle exposure induced inflammatory cytokine upregulation, inflammatory cell infiltration, antioxidant activity downregulation, and elevation of kidney injury molecule 1 (KIM-1) level in mouse kidneys. A dose-dependent effect of PM2.5 water extract and insoluble particle exposure on angiotensin converter enzyme 2 downregulation in mouse kidneys was observed.
We found that water-soluble extract and insoluble particles of PM2.5 could induce oxidative stress and inflammatory reactions, influence the regulation of renin-angiotensin system (RAS), and lead to kidney injury marker level elevation in mouse kidneys. The lowest-observed-adverse-effect level for renal toxicity in mice was 40 μg water-soluble extract/insoluble particle inhalation per week, which was approximately equal to the ambient PM2.5 concentration of 44 μg/m3 for mice.
[Display omitted]
•PM2.5 collected at the Kaohsiung industrial complex was chemically analyzed.•Water extracts and insoluble particles of PM2.5 induced inflammatory cell infiltration in mouse kidneys.•W PM2.5 induced angiotensin-converting enzyme 2 downregulation in mouse kidney.•PM2.5 induced antioxidant activity downregulation.•Water extracts and insoluble particle induced apoptosis expression.</description><identifier>ISSN: 0048-9697</identifier><identifier>EISSN: 1879-1026</identifier><identifier>DOI: 10.1016/j.scitotenv.2022.157528</identifier><language>eng</language><publisher>Elsevier B.V</publisher><subject>ACE ; Air pollution ; Angiotensin converter enzyme ; Apoptosis ; Fine particulate matter ; Inflammatory ; Mice kidney ; Oxidative stress ; PM2.5</subject><ispartof>The Science of the total environment, 2022-11, Vol.847, p.157528-157528, Article 157528</ispartof><rights>2022 The Authors</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c397t-d30c34f3058fcb502d6d3d33732e7e125ab50e8be1a4ad66ba3d9d539a4ee6283</citedby><cites>FETCH-LOGICAL-c397t-d30c34f3058fcb502d6d3d33732e7e125ab50e8be1a4ad66ba3d9d539a4ee6283</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.scitotenv.2022.157528$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3548,27922,27923,45993</link.rule.ids></links><search><creatorcontrib>Yuan, Chung-Shin</creatorcontrib><creatorcontrib>Lai, Ching-Shu</creatorcontrib><creatorcontrib>Chang-Chien, Guo-Ping</creatorcontrib><creatorcontrib>Tseng, Yu-Lun</creatorcontrib><creatorcontrib>Cheng, Fu-Jen</creatorcontrib><title>Kidney damage induced by repeated fine particulate matter exposure: Effects of different components</title><title>The Science of the total environment</title><description>Exposure to fine particulate matter with an aerodynamic diameter of ≤2.5 μm (PM2.5) is associated with adverse health effects. This study aimed to evaluate the toxic effects of the constituents of PM2.5 on mouse kidneys.
We collected PM2.5 near an industrial complex located in southern Kaohsiung, Taiwan, that was divided into water extract and insoluble particles. Male C57BL/6 mice were divided into five groups: control, low- and high-dose insoluble particle exposure, and low- and high-dose water extract exposure. Biochemical analysis, Western blot analysis, histological examination, and immunohistochemistry were performed to evaluate the impact of PM2.5 constituents on mice kidneys.
PM2.5 was collected from January 1, 2021, to February 8, 2021, from an industrial complex in Kaohsiung, Taiwan. Metallic element analysis showed that Pb, Ni, V, and Ti were non-essential metals with enrichment factors >10. Polycyclic aromatic hydrocarbon and nitrate polycyclic aromatic hydrocarbon analyses revealed that the toxic equivalents are, in the order, benzo(a)pyrene (BaP), indeno(1,2,3-cd) pyrene (IP), dibenzo(a,h)anthracene (DBA), and benzo(b)fluoranthene (BbF), which are potential carcinogens. Both water extract and insoluble particle exposure induced inflammatory cytokine upregulation, inflammatory cell infiltration, antioxidant activity downregulation, and elevation of kidney injury molecule 1 (KIM-1) level in mouse kidneys. A dose-dependent effect of PM2.5 water extract and insoluble particle exposure on angiotensin converter enzyme 2 downregulation in mouse kidneys was observed.
We found that water-soluble extract and insoluble particles of PM2.5 could induce oxidative stress and inflammatory reactions, influence the regulation of renin-angiotensin system (RAS), and lead to kidney injury marker level elevation in mouse kidneys. The lowest-observed-adverse-effect level for renal toxicity in mice was 40 μg water-soluble extract/insoluble particle inhalation per week, which was approximately equal to the ambient PM2.5 concentration of 44 μg/m3 for mice.
[Display omitted]
•PM2.5 collected at the Kaohsiung industrial complex was chemically analyzed.•Water extracts and insoluble particles of PM2.5 induced inflammatory cell infiltration in mouse kidneys.•W PM2.5 induced angiotensin-converting enzyme 2 downregulation in mouse kidney.•PM2.5 induced antioxidant activity downregulation.•Water extracts and insoluble particle induced apoptosis expression.</description><subject>ACE</subject><subject>Air pollution</subject><subject>Angiotensin converter enzyme</subject><subject>Apoptosis</subject><subject>Fine particulate matter</subject><subject>Inflammatory</subject><subject>Mice kidney</subject><subject>Oxidative stress</subject><subject>PM2.5</subject><issn>0048-9697</issn><issn>1879-1026</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><recordid>eNqFkEtPwzAQhC0EEqXwG_CRS4IfiZNwq6ryEJW4wNly7A1ylcTBdir673FVxJW97Gg0s9J-CN1SklNCxf0uD9pGF2Hc54wwltOyKll9hha0rpqMEibO0YKQos4a0VSX6CqEHUlT1XSB9Ks1IxywUYP6BGxHM2swuD1gDxOomHRnR8CT8tHquU8OHlSM4DF8Ty7MHh7wputAx4Bdh41N2sMYsXbD5MakwjW66FQf4OZ3L9HH4-Z9_Zxt355e1qttpnlTxcxwonnRcVLWnW5Lwoww3HBecQYVUFaqZELdAlWFMkK0ipvGlLxRBYBgNV-iu9PdybuvGUKUgw0a-l6N4OYgmWgSGJbopGh1imrvQvDQycnbQfmDpEQescqd_MMqj1jlCWtqrk5NSJ_sLfhjDsYEzfoEQRpn_73xAw1Zh30</recordid><startdate>20221115</startdate><enddate>20221115</enddate><creator>Yuan, Chung-Shin</creator><creator>Lai, Ching-Shu</creator><creator>Chang-Chien, Guo-Ping</creator><creator>Tseng, Yu-Lun</creator><creator>Cheng, Fu-Jen</creator><general>Elsevier B.V</general><scope>6I.</scope><scope>AAFTH</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20221115</creationdate><title>Kidney damage induced by repeated fine particulate matter exposure: Effects of different components</title><author>Yuan, Chung-Shin ; Lai, Ching-Shu ; Chang-Chien, Guo-Ping ; Tseng, Yu-Lun ; Cheng, Fu-Jen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c397t-d30c34f3058fcb502d6d3d33732e7e125ab50e8be1a4ad66ba3d9d539a4ee6283</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>ACE</topic><topic>Air pollution</topic><topic>Angiotensin converter enzyme</topic><topic>Apoptosis</topic><topic>Fine particulate matter</topic><topic>Inflammatory</topic><topic>Mice kidney</topic><topic>Oxidative stress</topic><topic>PM2.5</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yuan, Chung-Shin</creatorcontrib><creatorcontrib>Lai, Ching-Shu</creatorcontrib><creatorcontrib>Chang-Chien, Guo-Ping</creatorcontrib><creatorcontrib>Tseng, Yu-Lun</creatorcontrib><creatorcontrib>Cheng, Fu-Jen</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>The Science of the total environment</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yuan, Chung-Shin</au><au>Lai, Ching-Shu</au><au>Chang-Chien, Guo-Ping</au><au>Tseng, Yu-Lun</au><au>Cheng, Fu-Jen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Kidney damage induced by repeated fine particulate matter exposure: Effects of different components</atitle><jtitle>The Science of the total environment</jtitle><date>2022-11-15</date><risdate>2022</risdate><volume>847</volume><spage>157528</spage><epage>157528</epage><pages>157528-157528</pages><artnum>157528</artnum><issn>0048-9697</issn><eissn>1879-1026</eissn><abstract>Exposure to fine particulate matter with an aerodynamic diameter of ≤2.5 μm (PM2.5) is associated with adverse health effects. This study aimed to evaluate the toxic effects of the constituents of PM2.5 on mouse kidneys.
We collected PM2.5 near an industrial complex located in southern Kaohsiung, Taiwan, that was divided into water extract and insoluble particles. Male C57BL/6 mice were divided into five groups: control, low- and high-dose insoluble particle exposure, and low- and high-dose water extract exposure. Biochemical analysis, Western blot analysis, histological examination, and immunohistochemistry were performed to evaluate the impact of PM2.5 constituents on mice kidneys.
PM2.5 was collected from January 1, 2021, to February 8, 2021, from an industrial complex in Kaohsiung, Taiwan. Metallic element analysis showed that Pb, Ni, V, and Ti were non-essential metals with enrichment factors >10. Polycyclic aromatic hydrocarbon and nitrate polycyclic aromatic hydrocarbon analyses revealed that the toxic equivalents are, in the order, benzo(a)pyrene (BaP), indeno(1,2,3-cd) pyrene (IP), dibenzo(a,h)anthracene (DBA), and benzo(b)fluoranthene (BbF), which are potential carcinogens. Both water extract and insoluble particle exposure induced inflammatory cytokine upregulation, inflammatory cell infiltration, antioxidant activity downregulation, and elevation of kidney injury molecule 1 (KIM-1) level in mouse kidneys. A dose-dependent effect of PM2.5 water extract and insoluble particle exposure on angiotensin converter enzyme 2 downregulation in mouse kidneys was observed.
We found that water-soluble extract and insoluble particles of PM2.5 could induce oxidative stress and inflammatory reactions, influence the regulation of renin-angiotensin system (RAS), and lead to kidney injury marker level elevation in mouse kidneys. The lowest-observed-adverse-effect level for renal toxicity in mice was 40 μg water-soluble extract/insoluble particle inhalation per week, which was approximately equal to the ambient PM2.5 concentration of 44 μg/m3 for mice.
[Display omitted]
•PM2.5 collected at the Kaohsiung industrial complex was chemically analyzed.•Water extracts and insoluble particles of PM2.5 induced inflammatory cell infiltration in mouse kidneys.•W PM2.5 induced angiotensin-converting enzyme 2 downregulation in mouse kidney.•PM2.5 induced antioxidant activity downregulation.•Water extracts and insoluble particle induced apoptosis expression.</abstract><pub>Elsevier B.V</pub><doi>10.1016/j.scitotenv.2022.157528</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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source | ScienceDirect Journals (5 years ago - present) |
subjects | ACE Air pollution Angiotensin converter enzyme Apoptosis Fine particulate matter Inflammatory Mice kidney Oxidative stress PM2.5 |
title | Kidney damage induced by repeated fine particulate matter exposure: Effects of different components |
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