Effects of chronic Cr and Ni co-exposure on liver inflammation and autophagy in mice by regulating the TLR4/mTOR pathway
Exposure to Cr and/or Ni can have widespread implications on the environment and health. However, the specific toxic effects of chronic Cr and Ni co-exposure on mice liver have not been reported. To ascertain the combined toxic effects of chronic Cr and Ni co-exposure on liver damage in mice, 80 6-w...
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| description | Exposure to Cr and/or Ni can have widespread implications on the environment and health. However, the specific toxic effects of chronic Cr and Ni co-exposure on mice liver have not been reported. To ascertain the combined toxic effects of chronic Cr and Ni co-exposure on liver damage in mice, 80 6-week-old female C57BL/6 J mice were randomly divided into 4 groups: the Con group, Cr group (Cr+6 50 mg/L), Ni group (Ni+2 110 mg/L), and Cr + Ni group (Cr+6 50 mg/L + Ni+2 110 mg/L). The trial period lasted for 16 weeks. The results showed that Cr+6 and/or Ni+2 increased liver weight and liver index (P |
| doi_str_mv | 10.1016/j.scitotenv.2024.171921 |
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•Chronic Cr and Ni co-exposure induces inflammation and autophagy in mice liver.•Cr and/or Ni activate the TLR4/mTOR pathway to promote liver damage in mice.•Chronic Cr and Ni co-exposure induces antagonistic effects on mice liver.</description><identifier>ISSN: 0048-9697</identifier><identifier>EISSN: 1879-1026</identifier><identifier>DOI: 10.1016/j.scitotenv.2024.171921</identifier><identifier>PMID: 38522525</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Autophagy ; Chromium ; environment ; factor analysis ; Female ; females ; gene expression ; histology ; inflammation ; Inflammation - chemically induced ; interleukin-6 ; Interleukin-6 - metabolism ; liver ; Liver - metabolism ; Liver toxic effect ; Mice ; Mice, Inbred C57BL ; Myeloid Differentiation Factor 88 - metabolism ; NF-kappa B ; Nickel ; protein synthesis ; RNA, Messenger ; Signal Transduction ; TLR4/mTOR pathway ; TNF Receptor-Associated Factor 6 - metabolism ; TNF Receptor-Associated Factor 6 - pharmacology ; Toll-Like Receptor 4 - metabolism ; TOR Serine-Threonine Kinases - metabolism ; TOR Serine-Threonine Kinases - pharmacology ; toxicity ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>The Science of the total environment, 2024-05, Vol.926, p.171921-171921, Article 171921</ispartof><rights>2024 Elsevier B.V.</rights><rights>Copyright © 2024 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c350t-6219c703ff83905e318f6986b12a568510d2a3432c44ca9dee850e4a74eb50333</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.2024.171921$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38522525$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cao, Xianhong</creatorcontrib><creatorcontrib>Zheng, Shuangyan</creatorcontrib><creatorcontrib>Zeng, Yizhou</creatorcontrib><creatorcontrib>Shi, Yan</creatorcontrib><creatorcontrib>Du, Jun</creatorcontrib><creatorcontrib>Huang, Cheng</creatorcontrib><creatorcontrib>Shen, Yufan</creatorcontrib><creatorcontrib>Liu, Ping</creatorcontrib><creatorcontrib>Guo, Xiaoquan</creatorcontrib><creatorcontrib>Gao, Xiaona</creatorcontrib><title>Effects of chronic Cr and Ni co-exposure on liver inflammation and autophagy in mice by regulating the TLR4/mTOR pathway</title><title>The Science of the total environment</title><addtitle>Sci Total Environ</addtitle><description>Exposure to Cr and/or Ni can have widespread implications on the environment and health. However, the specific toxic effects of chronic Cr and Ni co-exposure on mice liver have not been reported. To ascertain the combined toxic effects of chronic Cr and Ni co-exposure on liver damage in mice, 80 6-week-old female C57BL/6 J mice were randomly divided into 4 groups: the Con group, Cr group (Cr+6 50 mg/L), Ni group (Ni+2 110 mg/L), and Cr + Ni group (Cr+6 50 mg/L + Ni+2 110 mg/L). The trial period lasted for 16 weeks. The results showed that Cr+6 and/or Ni+2 increased liver weight and liver index (P < 0.05) in mice, caused histological abnormality and ultrastructural damage, and micronutrients imbalance in mice liver. These findings serve as the basis for subsequent experiments. Compared with the individual exposure group, chronic Cr and Ni co-exposure resulted in decreased levels and activities of ALT, AST, MDA, T-AOC, and T-SOD (P < 0.05) in liver tissue, and decreased the mRNA expression levels of the TLR4/mTOR pathway related factors (TLR4, TRAM, TRIF, TBK-1, IRF-3, MyD88, IRAK-4, TRAF6, TAK-1, IKKβ, NF-κB, IL-1β, IL-6, TNFα, ULK1, Beclin 1, LC3) (P < 0.05) and decreased the protein expression levels of the factors (TLR4, MyD88, TRAF6, NF-κB p50, IL-6, TNFα, ULK1, LC3II/LC3I) (P < 0.05). Moreover, factorial analysis revealed the interaction between Cr and Ni, which was manifested as antagonistic effects on Cr concentration, Ni concentration, and TLR4, MyD88, NF-κB, mTOR, LC3, and p62 mRNA expression levels. In conclusion, the TLR4/mTOR pathway as a mechanism through which chronic Cr and Ni co-exposure induce liver inflammation and autophagy in mice, and there was an antagonistic effect between Cr and Ni. The above results provided a theoretical basis for understanding the underlying processes.
[Display omitted]
•Chronic Cr and Ni co-exposure induces inflammation and autophagy in mice liver.•Cr and/or Ni activate the TLR4/mTOR pathway to promote liver damage in mice.•Chronic Cr and Ni co-exposure induces antagonistic effects on mice liver.</description><subject>Animals</subject><subject>Autophagy</subject><subject>Chromium</subject><subject>environment</subject><subject>factor analysis</subject><subject>Female</subject><subject>females</subject><subject>gene expression</subject><subject>histology</subject><subject>inflammation</subject><subject>Inflammation - chemically induced</subject><subject>interleukin-6</subject><subject>Interleukin-6 - metabolism</subject><subject>liver</subject><subject>Liver - metabolism</subject><subject>Liver toxic effect</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Myeloid Differentiation Factor 88 - metabolism</subject><subject>NF-kappa B</subject><subject>Nickel</subject><subject>protein synthesis</subject><subject>RNA, Messenger</subject><subject>Signal Transduction</subject><subject>TLR4/mTOR pathway</subject><subject>TNF Receptor-Associated Factor 6 - metabolism</subject><subject>TNF Receptor-Associated Factor 6 - pharmacology</subject><subject>Toll-Like Receptor 4 - metabolism</subject><subject>TOR Serine-Threonine Kinases - metabolism</subject><subject>TOR Serine-Threonine Kinases - pharmacology</subject><subject>toxicity</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>0048-9697</issn><issn>1879-1026</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1v2zAMQIVhw5p1-wubjrs41YdlScci6NYCwQoU2VlQZCpRYFueJGfNv5-DdL2WFwLkIwnwIfSNkiUltLk5LLMLJRYYjktGWL2kkmpG36EFVVJXlLDmPVoQUqtKN1peoU85H8gcUtGP6IorwZhgYoGe77wHVzKOHrt9ikNweJWwHVr8K2AXK3geY54S4DjgLhwh4TD4zva9LWEunUE7lTju7e40t3AfHODtCSfYTd3MDDtc9oA366f6pt88PuHRlv1fe_qMPnjbZfjykq_R7x93m9V9tX78-bC6XVeOC1KqhlHtJOHeK66JAE6Vb7RqtpRZ0ShBScssrzlzde2sbgGUIFBbWcNWEM75Nfp-2Tum-GeCXEwfsoOuswPEKRtOBZeEKEbfRJlWQuqasWZG5QV1KeacwJsxhd6mk6HEnA2Zg3k1ZM6GzMXQPPn15ci07aF9nfuvZAZuLwDMXzkGSOdFMDhoQ5pNmTaGN4_8A1kmpWc</recordid><startdate>20240520</startdate><enddate>20240520</enddate><creator>Cao, Xianhong</creator><creator>Zheng, Shuangyan</creator><creator>Zeng, Yizhou</creator><creator>Shi, Yan</creator><creator>Du, Jun</creator><creator>Huang, Cheng</creator><creator>Shen, Yufan</creator><creator>Liu, Ping</creator><creator>Guo, Xiaoquan</creator><creator>Gao, Xiaona</creator><general>Elsevier B.V</general><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>7S9</scope><scope>L.6</scope></search><sort><creationdate>20240520</creationdate><title>Effects of chronic Cr and Ni co-exposure on liver inflammation and autophagy in mice by regulating the TLR4/mTOR pathway</title><author>Cao, Xianhong ; 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However, the specific toxic effects of chronic Cr and Ni co-exposure on mice liver have not been reported. To ascertain the combined toxic effects of chronic Cr and Ni co-exposure on liver damage in mice, 80 6-week-old female C57BL/6 J mice were randomly divided into 4 groups: the Con group, Cr group (Cr+6 50 mg/L), Ni group (Ni+2 110 mg/L), and Cr + Ni group (Cr+6 50 mg/L + Ni+2 110 mg/L). The trial period lasted for 16 weeks. The results showed that Cr+6 and/or Ni+2 increased liver weight and liver index (P < 0.05) in mice, caused histological abnormality and ultrastructural damage, and micronutrients imbalance in mice liver. These findings serve as the basis for subsequent experiments. Compared with the individual exposure group, chronic Cr and Ni co-exposure resulted in decreased levels and activities of ALT, AST, MDA, T-AOC, and T-SOD (P < 0.05) in liver tissue, and decreased the mRNA expression levels of the TLR4/mTOR pathway related factors (TLR4, TRAM, TRIF, TBK-1, IRF-3, MyD88, IRAK-4, TRAF6, TAK-1, IKKβ, NF-κB, IL-1β, IL-6, TNFα, ULK1, Beclin 1, LC3) (P < 0.05) and decreased the protein expression levels of the factors (TLR4, MyD88, TRAF6, NF-κB p50, IL-6, TNFα, ULK1, LC3II/LC3I) (P < 0.05). Moreover, factorial analysis revealed the interaction between Cr and Ni, which was manifested as antagonistic effects on Cr concentration, Ni concentration, and TLR4, MyD88, NF-κB, mTOR, LC3, and p62 mRNA expression levels. In conclusion, the TLR4/mTOR pathway as a mechanism through which chronic Cr and Ni co-exposure induce liver inflammation and autophagy in mice, and there was an antagonistic effect between Cr and Ni. The above results provided a theoretical basis for understanding the underlying processes.
[Display omitted]
•Chronic Cr and Ni co-exposure induces inflammation and autophagy in mice liver.•Cr and/or Ni activate the TLR4/mTOR pathway to promote liver damage in mice.•Chronic Cr and Ni co-exposure induces antagonistic effects on mice liver.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>38522525</pmid><doi>10.1016/j.scitotenv.2024.171921</doi><tpages>1</tpages></addata></record> |
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| subjects | Animals Autophagy Chromium environment factor analysis Female females gene expression histology inflammation Inflammation - chemically induced interleukin-6 Interleukin-6 - metabolism liver Liver - metabolism Liver toxic effect Mice Mice, Inbred C57BL Myeloid Differentiation Factor 88 - metabolism NF-kappa B Nickel protein synthesis RNA, Messenger Signal Transduction TLR4/mTOR pathway TNF Receptor-Associated Factor 6 - metabolism TNF Receptor-Associated Factor 6 - pharmacology Toll-Like Receptor 4 - metabolism TOR Serine-Threonine Kinases - metabolism TOR Serine-Threonine Kinases - pharmacology toxicity Tumor Necrosis Factor-alpha - metabolism |
| title | Effects of chronic Cr and Ni co-exposure on liver inflammation and autophagy in mice by regulating the TLR4/mTOR pathway |
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