Citreoviridin induces apoptosis through oxidative damage and inflammatory response in PC-12 cells
Citreoviridin (CIT) is a mycotoxin produced by various fungi. Although CIT has been reported to cause neurotoxicity, the molecular mechanism is poorly understood. Therefore, the aim of this study was to investigate the effects and molecular mechanisms of CIT in neurotoxicity. Different concentration...
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| Veröffentlicht in: | Toxicology and industrial health 2025-01, Vol.41 (1), p.32-39 |
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| creator | Yang, Jing Lu, Jiaojiao Cao, Luoyuan Dong, Wenxu Zheng, Xian Fu, Xianguo |
| description | Citreoviridin (CIT) is a mycotoxin produced by various fungi. Although CIT has been reported to cause neurotoxicity, the molecular mechanism is poorly understood. Therefore, the aim of this study was to investigate the effects and molecular mechanisms of CIT in neurotoxicity. Different concentrations of CIT were treated to rat pheochromocytoma (PC-12 cells), and oxidative stress parameters, cytokine levels, and cell apoptosis were evaluated. CIT treatment (5 and 10 μM) significantly induced PC-12 cell apoptosis and increased lactate dehydrogenase activity. Additionally, CIT treatment induced oxidative stress, as evidenced by a significant increase in intracellular levels of reactive oxygen species, malondialdehyde, and superoxide dismutase and a decrease in glutathione activity. Moreover, CIT treatment induced an inflammatory response, as evidenced by a significant increase in the intracellular levels of the proinflammatory cytokines tumor necrosis factor-alpha and interleukin-1-beta in PC-12 cells. Furthermore, quantitative PCR and western blotting showed that CIT treatment increased both the protein and mRNA expression of GADD45α and p21 in PC-12 cells, suggesting that CIT may induce apoptosis by inhibiting cell cycle, blocking cell growth, and damaging DNA. Conclusively, this study contributes the understanding the toxicity mechanisms of CIT to nerve cells. |
| doi_str_mv | 10.1177/07482337241295474 |
| format | Article |
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Although CIT has been reported to cause neurotoxicity, the molecular mechanism is poorly understood. Therefore, the aim of this study was to investigate the effects and molecular mechanisms of CIT in neurotoxicity. Different concentrations of CIT were treated to rat pheochromocytoma (PC-12 cells), and oxidative stress parameters, cytokine levels, and cell apoptosis were evaluated. CIT treatment (5 and 10 μM) significantly induced PC-12 cell apoptosis and increased lactate dehydrogenase activity. Additionally, CIT treatment induced oxidative stress, as evidenced by a significant increase in intracellular levels of reactive oxygen species, malondialdehyde, and superoxide dismutase and a decrease in glutathione activity. Moreover, CIT treatment induced an inflammatory response, as evidenced by a significant increase in the intracellular levels of the proinflammatory cytokines tumor necrosis factor-alpha and interleukin-1-beta in PC-12 cells. Furthermore, quantitative PCR and western blotting showed that CIT treatment increased both the protein and mRNA expression of GADD45α and p21 in PC-12 cells, suggesting that CIT may induce apoptosis by inhibiting cell cycle, blocking cell growth, and damaging DNA. Conclusively, this study contributes the understanding the toxicity mechanisms of CIT to nerve cells.</description><identifier>ISSN: 0748-2337</identifier><identifier>ISSN: 1477-0393</identifier><identifier>EISSN: 1477-0393</identifier><identifier>DOI: 10.1177/07482337241295474</identifier><identifier>PMID: 39437026</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Animals ; Apoptosis ; Apoptosis - drug effects ; Aurovertins - pharmacology ; Cell cycle ; Cell Cycle Proteins - metabolism ; Cytokines ; Damage ; DNA damage ; GADD45 Proteins ; Gene expression ; Glutathione ; Glutathione - metabolism ; GTP-binding protein ; Inflammation ; Inflammation - chemically induced ; Inflammatory response ; Interleukin 1 ; Interleukin-1beta - metabolism ; Intracellular ; Intracellular levels ; L-Lactate dehydrogenase ; Lactate dehydrogenase ; Malondialdehyde - metabolism ; Molecular modelling ; Mycotoxins ; Neurotoxicity ; Oxidative stress ; Oxidative Stress - drug effects ; PC12 Cells ; Rats ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Superoxide dismutase ; Superoxide Dismutase - metabolism ; Tumor Necrosis Factor-alpha - metabolism ; Western blotting</subject><ispartof>Toxicology and industrial health, 2025-01, Vol.41 (1), p.32-39</ispartof><rights>The Author(s) 2024</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c250t-6b9c5cd7f84ba40253cc252c1456e530c194a8ff0b1a8cc84759be7ff0e416333</cites><orcidid>0000-0003-2116-2474</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1177/07482337241295474$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1177/07482337241295474$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,776,780,21798,27901,27902,43597,43598</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39437026$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Jing</creatorcontrib><creatorcontrib>Lu, Jiaojiao</creatorcontrib><creatorcontrib>Cao, Luoyuan</creatorcontrib><creatorcontrib>Dong, Wenxu</creatorcontrib><creatorcontrib>Zheng, Xian</creatorcontrib><creatorcontrib>Fu, Xianguo</creatorcontrib><title>Citreoviridin induces apoptosis through oxidative damage and inflammatory response in PC-12 cells</title><title>Toxicology and industrial health</title><addtitle>Toxicol Ind Health</addtitle><description>Citreoviridin (CIT) is a mycotoxin produced by various fungi. Although CIT has been reported to cause neurotoxicity, the molecular mechanism is poorly understood. Therefore, the aim of this study was to investigate the effects and molecular mechanisms of CIT in neurotoxicity. Different concentrations of CIT were treated to rat pheochromocytoma (PC-12 cells), and oxidative stress parameters, cytokine levels, and cell apoptosis were evaluated. CIT treatment (5 and 10 μM) significantly induced PC-12 cell apoptosis and increased lactate dehydrogenase activity. Additionally, CIT treatment induced oxidative stress, as evidenced by a significant increase in intracellular levels of reactive oxygen species, malondialdehyde, and superoxide dismutase and a decrease in glutathione activity. Moreover, CIT treatment induced an inflammatory response, as evidenced by a significant increase in the intracellular levels of the proinflammatory cytokines tumor necrosis factor-alpha and interleukin-1-beta in PC-12 cells. Furthermore, quantitative PCR and western blotting showed that CIT treatment increased both the protein and mRNA expression of GADD45α and p21 in PC-12 cells, suggesting that CIT may induce apoptosis by inhibiting cell cycle, blocking cell growth, and damaging DNA. Conclusively, this study contributes the understanding the toxicity mechanisms of CIT to nerve cells.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Aurovertins - pharmacology</subject><subject>Cell cycle</subject><subject>Cell Cycle Proteins - metabolism</subject><subject>Cytokines</subject><subject>Damage</subject><subject>DNA damage</subject><subject>GADD45 Proteins</subject><subject>Gene expression</subject><subject>Glutathione</subject><subject>Glutathione - metabolism</subject><subject>GTP-binding protein</subject><subject>Inflammation</subject><subject>Inflammation - chemically induced</subject><subject>Inflammatory response</subject><subject>Interleukin 1</subject><subject>Interleukin-1beta - metabolism</subject><subject>Intracellular</subject><subject>Intracellular levels</subject><subject>L-Lactate dehydrogenase</subject><subject>Lactate dehydrogenase</subject><subject>Malondialdehyde - metabolism</subject><subject>Molecular modelling</subject><subject>Mycotoxins</subject><subject>Neurotoxicity</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>PC12 Cells</subject><subject>Rats</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Superoxide dismutase</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Western blotting</subject><issn>0748-2337</issn><issn>1477-0393</issn><issn>1477-0393</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2025</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kEtLxDAUhYMozjj6A9xIwI2bjnk2zVIGXyDoQtclTdOZDG1Tk3Zw_r0pMyoori6c891zLweAc4zmGAtxjQTLCKWCMEwkZ4IdgClmQiSISnoIpqOfjMAEnISwRgilKSfHYEIlowKRdArUwvbeuI31trQttG05aBOg6lzXu2AD7FfeDcsVdB-2VL3dGFiqRi0NVG0Z8apWTaN657fQm9C5NpiowpdFggnUpq7DKTiqVB3M2X7OwNvd7eviIXl6vn9c3DwlmnDUJ2khNdelqDJWKIYIpzoaRGPGU8Mp0lgylVUVKrDKtM6Y4LIwIgqG4ZRSOgNXu9zOu_fBhD5vbBg_UK1xQ8gpxlIQLDMU0ctf6NoNvo3fRYoRSoRgLFJ4R2nvQvCmyjtvG-W3OUb52H_-p_-4c7FPHorGlN8bX4VHYL4DQuzw5-z_iZ9-Dozc</recordid><startdate>202501</startdate><enddate>202501</enddate><creator>Yang, Jing</creator><creator>Lu, Jiaojiao</creator><creator>Cao, Luoyuan</creator><creator>Dong, Wenxu</creator><creator>Zheng, Xian</creator><creator>Fu, Xianguo</creator><general>SAGE Publications</general><general>Sage Publications Ltd</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>7QF</scope><scope>7QQ</scope><scope>7SC</scope><scope>7SE</scope><scope>7SP</scope><scope>7SR</scope><scope>7T2</scope><scope>7TA</scope><scope>7TB</scope><scope>7U5</scope><scope>7U7</scope><scope>8BQ</scope><scope>8FD</scope><scope>C1K</scope><scope>F28</scope><scope>FR3</scope><scope>H8D</scope><scope>H8G</scope><scope>JG9</scope><scope>JQ2</scope><scope>K9.</scope><scope>KR7</scope><scope>L7M</scope><scope>L~C</scope><scope>L~D</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-2116-2474</orcidid></search><sort><creationdate>202501</creationdate><title>Citreoviridin induces apoptosis through oxidative damage and inflammatory response in PC-12 cells</title><author>Yang, Jing ; Lu, Jiaojiao ; Cao, Luoyuan ; Dong, Wenxu ; Zheng, Xian ; Fu, Xianguo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c250t-6b9c5cd7f84ba40253cc252c1456e530c194a8ff0b1a8cc84759be7ff0e416333</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2025</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Aurovertins - pharmacology</topic><topic>Cell cycle</topic><topic>Cell Cycle Proteins - metabolism</topic><topic>Cytokines</topic><topic>Damage</topic><topic>DNA damage</topic><topic>GADD45 Proteins</topic><topic>Gene expression</topic><topic>Glutathione</topic><topic>Glutathione - metabolism</topic><topic>GTP-binding protein</topic><topic>Inflammation</topic><topic>Inflammation - chemically induced</topic><topic>Inflammatory response</topic><topic>Interleukin 1</topic><topic>Interleukin-1beta - metabolism</topic><topic>Intracellular</topic><topic>Intracellular levels</topic><topic>L-Lactate dehydrogenase</topic><topic>Lactate dehydrogenase</topic><topic>Malondialdehyde - metabolism</topic><topic>Molecular modelling</topic><topic>Mycotoxins</topic><topic>Neurotoxicity</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>PC12 Cells</topic><topic>Rats</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Superoxide dismutase</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Jing</creatorcontrib><creatorcontrib>Lu, Jiaojiao</creatorcontrib><creatorcontrib>Cao, Luoyuan</creatorcontrib><creatorcontrib>Dong, Wenxu</creatorcontrib><creatorcontrib>Zheng, Xian</creatorcontrib><creatorcontrib>Fu, Xianguo</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Aluminium Industry Abstracts</collection><collection>Ceramic Abstracts</collection><collection>Computer and Information Systems Abstracts</collection><collection>Corrosion Abstracts</collection><collection>Electronics & Communications Abstracts</collection><collection>Engineered Materials Abstracts</collection><collection>Health and Safety Science Abstracts (Full archive)</collection><collection>Materials Business File</collection><collection>Mechanical & Transportation Engineering Abstracts</collection><collection>Solid State and Superconductivity Abstracts</collection><collection>Toxicology Abstracts</collection><collection>METADEX</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ANTE: Abstracts in New Technology & Engineering</collection><collection>Engineering Research Database</collection><collection>Aerospace Database</collection><collection>Copper Technical Reference Library</collection><collection>Materials Research Database</collection><collection>ProQuest Computer Science Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Civil Engineering Abstracts</collection><collection>Advanced Technologies Database with Aerospace</collection><collection>Computer and Information Systems Abstracts Academic</collection><collection>Computer and Information Systems Abstracts Professional</collection><collection>MEDLINE - Academic</collection><jtitle>Toxicology and industrial health</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Jing</au><au>Lu, Jiaojiao</au><au>Cao, Luoyuan</au><au>Dong, Wenxu</au><au>Zheng, Xian</au><au>Fu, Xianguo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Citreoviridin induces apoptosis through oxidative damage and inflammatory response in PC-12 cells</atitle><jtitle>Toxicology and industrial health</jtitle><addtitle>Toxicol Ind Health</addtitle><date>2025-01</date><risdate>2025</risdate><volume>41</volume><issue>1</issue><spage>32</spage><epage>39</epage><pages>32-39</pages><issn>0748-2337</issn><issn>1477-0393</issn><eissn>1477-0393</eissn><abstract>Citreoviridin (CIT) is a mycotoxin produced by various fungi. Although CIT has been reported to cause neurotoxicity, the molecular mechanism is poorly understood. Therefore, the aim of this study was to investigate the effects and molecular mechanisms of CIT in neurotoxicity. Different concentrations of CIT were treated to rat pheochromocytoma (PC-12 cells), and oxidative stress parameters, cytokine levels, and cell apoptosis were evaluated. CIT treatment (5 and 10 μM) significantly induced PC-12 cell apoptosis and increased lactate dehydrogenase activity. Additionally, CIT treatment induced oxidative stress, as evidenced by a significant increase in intracellular levels of reactive oxygen species, malondialdehyde, and superoxide dismutase and a decrease in glutathione activity. Moreover, CIT treatment induced an inflammatory response, as evidenced by a significant increase in the intracellular levels of the proinflammatory cytokines tumor necrosis factor-alpha and interleukin-1-beta in PC-12 cells. Furthermore, quantitative PCR and western blotting showed that CIT treatment increased both the protein and mRNA expression of GADD45α and p21 in PC-12 cells, suggesting that CIT may induce apoptosis by inhibiting cell cycle, blocking cell growth, and damaging DNA. Conclusively, this study contributes the understanding the toxicity mechanisms of CIT to nerve cells.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>39437026</pmid><doi>10.1177/07482337241295474</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0003-2116-2474</orcidid></addata></record> |
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| subjects | Animals Apoptosis Apoptosis - drug effects Aurovertins - pharmacology Cell cycle Cell Cycle Proteins - metabolism Cytokines Damage DNA damage GADD45 Proteins Gene expression Glutathione Glutathione - metabolism GTP-binding protein Inflammation Inflammation - chemically induced Inflammatory response Interleukin 1 Interleukin-1beta - metabolism Intracellular Intracellular levels L-Lactate dehydrogenase Lactate dehydrogenase Malondialdehyde - metabolism Molecular modelling Mycotoxins Neurotoxicity Oxidative stress Oxidative Stress - drug effects PC12 Cells Rats Reactive oxygen species Reactive Oxygen Species - metabolism Superoxide dismutase Superoxide Dismutase - metabolism Tumor Necrosis Factor-alpha - metabolism Western blotting |
| title | Citreoviridin induces apoptosis through oxidative damage and inflammatory response in PC-12 cells |
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