Trace elements and metal nanoparticles: mechanistic approaches to mitigating chemotherapy-induced toxicity—a review of literature evidence
Anticancer chemotherapy (ACT) remains a cornerstone in cancer treatment, despite significant advances in pharmacology over recent decades. However, its associated side effect toxicity continues to pose a major concern for both oncology clinicians and patients, significantly impacting treatment proto...
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| Veröffentlicht in: | Biometals 2024-12, Vol.37 (6), p.1325-1378 |
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| creator | Famurewa, Ademola C. George, Mina Y. Ukwubile, Cletus A. Kumar, Sachindra Kamal, Mehta V. Belle, Vijetha S. Othman, Eman M. Pai, Sreedhara Ranganath K. |
| description | Anticancer chemotherapy (ACT) remains a cornerstone in cancer treatment, despite significant advances in pharmacology over recent decades. However, its associated side effect toxicity continues to pose a major concern for both oncology clinicians and patients, significantly impacting treatment protocols and patient quality of life. Current clinical strategies to mitigate ACT-induced toxicity have proven largely unsatisfactory, leaving a critical unmet need to block toxicity mechanisms without diminishing ACT's therapeutic efficacy. This review aims to document the molecular mechanisms underlying ACT toxicity and highlight research efforts exploring the protective effects of trace elements (TEs) and their nanoparticles (NPs) against these mechanisms. Our literature review reveals that the primary driver of ACT toxicity is redox imbalance, which triggers oxidative inflammation, apoptosis, endoplasmic reticulum stress, mitochondrial dysfunction, autophagy, and dysregulation of signaling pathways such as PI3K/mTOR/Akt. Studies suggest that TEs, including zinc, selenium, boron, manganese, and molybdenum, and their NPs, can potentially counteract ACT-induced toxicity by inhibiting oxidative stress-mediated pathways, including NF-κB/TLR4/MAPK/NLRP3, STAT-3/NLRP3, Bcl-2/Bid/p53/caspases, and LC3/Beclin-1/CHOP/ATG6, while also upregulating protective signaling pathways like Sirt1/PPAR-γ/PGC-1α/FOXO-3 and Nrf2/HO-1/ARE. However, evidence regarding the roles of lncRNA and the Wnt/β-catenin pathway in ACT toxicity remains inconsistent, and the impact of TEs and NPs on ACT efficacy is not fully understood. Further research is needed to confirm the protective effects of TEs and their NPs against ACT toxicity in cancer patients. In summary, TEs and their NPs present a promising avenue as adjuvant agents for preventing non-target organ toxicity induced by ACT. |
| doi_str_mv | 10.1007/s10534-024-00637-7 |
| format | Article |
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However, its associated side effect toxicity continues to pose a major concern for both oncology clinicians and patients, significantly impacting treatment protocols and patient quality of life. Current clinical strategies to mitigate ACT-induced toxicity have proven largely unsatisfactory, leaving a critical unmet need to block toxicity mechanisms without diminishing ACT's therapeutic efficacy. This review aims to document the molecular mechanisms underlying ACT toxicity and highlight research efforts exploring the protective effects of trace elements (TEs) and their nanoparticles (NPs) against these mechanisms. Our literature review reveals that the primary driver of ACT toxicity is redox imbalance, which triggers oxidative inflammation, apoptosis, endoplasmic reticulum stress, mitochondrial dysfunction, autophagy, and dysregulation of signaling pathways such as PI3K/mTOR/Akt. Studies suggest that TEs, including zinc, selenium, boron, manganese, and molybdenum, and their NPs, can potentially counteract ACT-induced toxicity by inhibiting oxidative stress-mediated pathways, including NF-κB/TLR4/MAPK/NLRP3, STAT-3/NLRP3, Bcl-2/Bid/p53/caspases, and LC3/Beclin-1/CHOP/ATG6, while also upregulating protective signaling pathways like Sirt1/PPAR-γ/PGC-1α/FOXO-3 and Nrf2/HO-1/ARE. However, evidence regarding the roles of lncRNA and the Wnt/β-catenin pathway in ACT toxicity remains inconsistent, and the impact of TEs and NPs on ACT efficacy is not fully understood. Further research is needed to confirm the protective effects of TEs and their NPs against ACT toxicity in cancer patients. In summary, TEs and their NPs present a promising avenue as adjuvant agents for preventing non-target organ toxicity induced by ACT.</description><identifier>ISSN: 0966-0844</identifier><identifier>ISSN: 1572-8773</identifier><identifier>EISSN: 1572-8773</identifier><identifier>DOI: 10.1007/s10534-024-00637-7</identifier><identifier>PMID: 39347848</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Animals ; Antineoplastic Agents - chemistry ; Antineoplastic Agents - pharmacology ; Apoptosis ; Autophagy ; Bcl-2 protein ; Biochemistry ; Biomedical and Life Sciences ; Boron ; Cancer therapies ; Cell Biology ; Chemotherapy ; Effectiveness ; Endoplasmic reticulum ; Forkhead protein ; Humans ; Life Sciences ; Literature reviews ; Manganese ; MAP kinase ; Medicine/Public Health ; Metal Nanoparticles - chemistry ; Microbiology ; Molecular modelling ; Molybdenum ; Nanoparticles ; Neoplasms - drug therapy ; Neoplasms - metabolism ; Neoplasms - pathology ; NF-κB protein ; Oxidative stress ; Oxidative Stress - drug effects ; Patients ; Pharmacology ; Pharmacology/Toxicology ; Plant Physiology ; Quality of life ; Review ; Selenium ; Signal transduction ; TLR4 protein ; Toxicity ; Trace elements ; Trace Elements - pharmacology ; Wnt protein ; β-Catenin</subject><ispartof>Biometals, 2024-12, Vol.37 (6), p.1325-1378</ispartof><rights>The Author(s), under exclusive licence to Springer Nature B.V. 2024 Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2024. The Author(s), under exclusive licence to Springer Nature B.V.</rights><rights>Copyright Springer Nature B.V. Dec 2024</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c256t-1dd75f1bde20bbdaf275a2be7a4908735f01dcdf2027b0dd3fd1b99420e12ba33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10534-024-00637-7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10534-024-00637-7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39347848$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Famurewa, Ademola C.</creatorcontrib><creatorcontrib>George, Mina Y.</creatorcontrib><creatorcontrib>Ukwubile, Cletus A.</creatorcontrib><creatorcontrib>Kumar, Sachindra</creatorcontrib><creatorcontrib>Kamal, Mehta V.</creatorcontrib><creatorcontrib>Belle, Vijetha S.</creatorcontrib><creatorcontrib>Othman, Eman M.</creatorcontrib><creatorcontrib>Pai, Sreedhara Ranganath K.</creatorcontrib><title>Trace elements and metal nanoparticles: mechanistic approaches to mitigating chemotherapy-induced toxicity—a review of literature evidence</title><title>Biometals</title><addtitle>Biometals</addtitle><addtitle>Biometals</addtitle><description>Anticancer chemotherapy (ACT) remains a cornerstone in cancer treatment, despite significant advances in pharmacology over recent decades. However, its associated side effect toxicity continues to pose a major concern for both oncology clinicians and patients, significantly impacting treatment protocols and patient quality of life. Current clinical strategies to mitigate ACT-induced toxicity have proven largely unsatisfactory, leaving a critical unmet need to block toxicity mechanisms without diminishing ACT's therapeutic efficacy. This review aims to document the molecular mechanisms underlying ACT toxicity and highlight research efforts exploring the protective effects of trace elements (TEs) and their nanoparticles (NPs) against these mechanisms. Our literature review reveals that the primary driver of ACT toxicity is redox imbalance, which triggers oxidative inflammation, apoptosis, endoplasmic reticulum stress, mitochondrial dysfunction, autophagy, and dysregulation of signaling pathways such as PI3K/mTOR/Akt. Studies suggest that TEs, including zinc, selenium, boron, manganese, and molybdenum, and their NPs, can potentially counteract ACT-induced toxicity by inhibiting oxidative stress-mediated pathways, including NF-κB/TLR4/MAPK/NLRP3, STAT-3/NLRP3, Bcl-2/Bid/p53/caspases, and LC3/Beclin-1/CHOP/ATG6, while also upregulating protective signaling pathways like Sirt1/PPAR-γ/PGC-1α/FOXO-3 and Nrf2/HO-1/ARE. However, evidence regarding the roles of lncRNA and the Wnt/β-catenin pathway in ACT toxicity remains inconsistent, and the impact of TEs and NPs on ACT efficacy is not fully understood. Further research is needed to confirm the protective effects of TEs and their NPs against ACT toxicity in cancer patients. In summary, TEs and their NPs present a promising avenue as adjuvant agents for preventing non-target organ toxicity induced by ACT.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Animals</subject><subject>Antineoplastic Agents - chemistry</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Bcl-2 protein</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Boron</subject><subject>Cancer therapies</subject><subject>Cell Biology</subject><subject>Chemotherapy</subject><subject>Effectiveness</subject><subject>Endoplasmic reticulum</subject><subject>Forkhead protein</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>Literature reviews</subject><subject>Manganese</subject><subject>MAP kinase</subject><subject>Medicine/Public Health</subject><subject>Metal Nanoparticles - chemistry</subject><subject>Microbiology</subject><subject>Molecular modelling</subject><subject>Molybdenum</subject><subject>Nanoparticles</subject><subject>Neoplasms - drug therapy</subject><subject>Neoplasms - metabolism</subject><subject>Neoplasms - pathology</subject><subject>NF-κB protein</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Patients</subject><subject>Pharmacology</subject><subject>Pharmacology/Toxicology</subject><subject>Plant Physiology</subject><subject>Quality of life</subject><subject>Review</subject><subject>Selenium</subject><subject>Signal transduction</subject><subject>TLR4 protein</subject><subject>Toxicity</subject><subject>Trace elements</subject><subject>Trace Elements - pharmacology</subject><subject>Wnt protein</subject><subject>β-Catenin</subject><issn>0966-0844</issn><issn>1572-8773</issn><issn>1572-8773</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc9u1DAQxi0EosvCC3BAlrhwCR3bSZxwQxX_pEq9lHM0sSe7rhIn2E7L3ngAjjwhT4LpFpA49GBZnvnNNzP-GHsu4LUA0KdRQKXKAmQ-UCtd6AdsIyoti0Zr9ZBtoK3rApqyPGFPYrwCgFZD_ZidqFaVuimbDft-GdAQp5Em8ily9JZPlHDkHv28YEjOjBTf5KDZo3cxvzkuS5jR7CnyNPPJJbfD5PyO59A0pz0FXA6F83Y1ZDPy1RmXDj-__UAe6NrRDZ8HPrqUubSG3P3aWfKGnrJHA46Rnt3dW_b5_bvLs4_F-cWHT2dvzwsjqzoVwlpdDaK3JKHvLQ5SVyh70li20GhVDSCssYMEqXuwVg1W9G1bSiAhe1Rqy14ddfMaX1aKqZtcNDSO6GleY6eEEBLqOn_vlr38D72a1-DzdJkqQVcNyDZT8kiZMMcYaOiW4CYMh05A99ur7uhVl73qbr3qdC56cSe99hPZvyV_zMmAOgIxp_yOwr_e98j-AvB6o9A</recordid><startdate>20241201</startdate><enddate>20241201</enddate><creator>Famurewa, Ademola C.</creator><creator>George, Mina Y.</creator><creator>Ukwubile, Cletus A.</creator><creator>Kumar, Sachindra</creator><creator>Kamal, Mehta V.</creator><creator>Belle, Vijetha S.</creator><creator>Othman, Eman M.</creator><creator>Pai, Sreedhara Ranganath K.</creator><general>Springer Netherlands</general><general>Springer Nature 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>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7U5</scope><scope>7U7</scope><scope>8BQ</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>JG9</scope><scope>K9.</scope><scope>L7M</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20241201</creationdate><title>Trace elements and metal nanoparticles: mechanistic approaches to mitigating chemotherapy-induced toxicity—a review of literature evidence</title><author>Famurewa, Ademola C. ; 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However, its associated side effect toxicity continues to pose a major concern for both oncology clinicians and patients, significantly impacting treatment protocols and patient quality of life. Current clinical strategies to mitigate ACT-induced toxicity have proven largely unsatisfactory, leaving a critical unmet need to block toxicity mechanisms without diminishing ACT's therapeutic efficacy. This review aims to document the molecular mechanisms underlying ACT toxicity and highlight research efforts exploring the protective effects of trace elements (TEs) and their nanoparticles (NPs) against these mechanisms. Our literature review reveals that the primary driver of ACT toxicity is redox imbalance, which triggers oxidative inflammation, apoptosis, endoplasmic reticulum stress, mitochondrial dysfunction, autophagy, and dysregulation of signaling pathways such as PI3K/mTOR/Akt. Studies suggest that TEs, including zinc, selenium, boron, manganese, and molybdenum, and their NPs, can potentially counteract ACT-induced toxicity by inhibiting oxidative stress-mediated pathways, including NF-κB/TLR4/MAPK/NLRP3, STAT-3/NLRP3, Bcl-2/Bid/p53/caspases, and LC3/Beclin-1/CHOP/ATG6, while also upregulating protective signaling pathways like Sirt1/PPAR-γ/PGC-1α/FOXO-3 and Nrf2/HO-1/ARE. However, evidence regarding the roles of lncRNA and the Wnt/β-catenin pathway in ACT toxicity remains inconsistent, and the impact of TEs and NPs on ACT efficacy is not fully understood. Further research is needed to confirm the protective effects of TEs and their NPs against ACT toxicity in cancer patients. In summary, TEs and their NPs present a promising avenue as adjuvant agents for preventing non-target organ toxicity induced by ACT.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>39347848</pmid><doi>10.1007/s10534-024-00637-7</doi><tpages>54</tpages></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Animals Antineoplastic Agents - chemistry Antineoplastic Agents - pharmacology Apoptosis Autophagy Bcl-2 protein Biochemistry Biomedical and Life Sciences Boron Cancer therapies Cell Biology Chemotherapy Effectiveness Endoplasmic reticulum Forkhead protein Humans Life Sciences Literature reviews Manganese MAP kinase Medicine/Public Health Metal Nanoparticles - chemistry Microbiology Molecular modelling Molybdenum Nanoparticles Neoplasms - drug therapy Neoplasms - metabolism Neoplasms - pathology NF-κB protein Oxidative stress Oxidative Stress - drug effects Patients Pharmacology Pharmacology/Toxicology Plant Physiology Quality of life Review Selenium Signal transduction TLR4 protein Toxicity Trace elements Trace Elements - pharmacology Wnt protein β-Catenin |
| title | Trace elements and metal nanoparticles: mechanistic approaches to mitigating chemotherapy-induced toxicity—a review of literature evidence |
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