Cadmium-induced neurotoxicity: still much ado
Cadmium (Cd) is a highly toxic heavy metal that accumulates in living system and as such is currently one of the most important occupational and environmental pollutants. Cd reaches into the environment by anthropogenic mobilization and it is absorbed from tobacco consumption or ingestion of contami...
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| Veröffentlicht in: | Neural regeneration research 2018-11, Vol.13 (11), p.1879-1882 |
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| creator | Branca, Jacopo Junio Valerio Morucci, Gabriele Pacini, Alessandra |
| description | Cadmium (Cd) is a highly toxic heavy metal that accumulates in living system and as such is currently one of the most important occupational and environmental pollutants. Cd reaches into the environment by anthropogenic mobilization and it is absorbed from tobacco consumption or ingestion of contaminated substances. Its extremely long biological half-life (approximately 20-30 years in humans) and low rate of excretion from the body cause cadmium storage predominantly in soft tissues (primarily, liver and kidneys) with a diversity of toxic effects such as nephrotoxicity, hepatotoxicity, endocrine and reproductive toxicities. Moreover, a Cd-dependent neurotoxicity has been also related to neurodegenerative diseases such as Alzheimer's and Parkinson's diseases, amyotrophic lateral sclerosis, and multiple sclerosis. At the cellular level, Cd affects cell proliferation, differentiation, apoptosis and other cellular activities. Among all these mechanisms, the Cd-dependent interference in DNA repair mechanisms as well as the generation of reactive oxygen species, seem to be the most important causes of its cellular toxicity. Nevertheless, there is still much to find out about its mechanisms of action and ways to reduce health risks. This article gives a brief review of the relevant mechanisms that it would be worth investigating in order to deep inside cadmium toxicity. |
| doi_str_mv | 10.4103/1673-5374.239434 |
| format | Article |
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Cd reaches into the environment by anthropogenic mobilization and it is absorbed from tobacco consumption or ingestion of contaminated substances. Its extremely long biological half-life (approximately 20-30 years in humans) and low rate of excretion from the body cause cadmium storage predominantly in soft tissues (primarily, liver and kidneys) with a diversity of toxic effects such as nephrotoxicity, hepatotoxicity, endocrine and reproductive toxicities. Moreover, a Cd-dependent neurotoxicity has been also related to neurodegenerative diseases such as Alzheimer's and Parkinson's diseases, amyotrophic lateral sclerosis, and multiple sclerosis. At the cellular level, Cd affects cell proliferation, differentiation, apoptosis and other cellular activities. Among all these mechanisms, the Cd-dependent interference in DNA repair mechanisms as well as the generation of reactive oxygen species, seem to be the most important causes of its cellular toxicity. Nevertheless, there is still much to find out about its mechanisms of action and ways to reduce health risks. This article gives a brief review of the relevant mechanisms that it would be worth investigating in order to deep inside cadmium toxicity.</description><identifier>ISSN: 1673-5374</identifier><identifier>EISSN: 1876-7958</identifier><identifier>DOI: 10.4103/1673-5374.239434</identifier><identifier>PMID: 30233056</identifier><language>eng</language><publisher>India: Medknow Publications and Media Pvt. Ltd</publisher><subject>Antioxidants ; Binding sites ; Cadmium ; Cell cycle ; Chemical properties ; Cytotoxicity ; Deoxyribonucleic acid ; Disease ; DNA ; DNA methylation ; Environmental aspects ; Enzymes ; Gene expression ; Hazardous materials ; Health aspects ; Hypotheses ; Neurotoxicity ; Oxidative stress ; Physiological aspects ; Reactive oxygen species ; Review ; Smoking</subject><ispartof>Neural regeneration research, 2018-11, Vol.13 (11), p.1879-1882</ispartof><rights>COPYRIGHT 2018 Medknow Publications and Media Pvt. Ltd.</rights><rights>2018. This article is published under (http://creativecommons.org/licenses/by-nc-sa/3.0/) (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Copyright © Wanfang Data Co. Ltd. All Rights Reserved.</rights><rights>Copyright: © Neural Regeneration Research 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c527t-d068e58cae3eb619c28e431d98f8e4f191b4c619f3f2df41ccd8e231f7582fbf3</citedby><cites>FETCH-LOGICAL-c527t-d068e58cae3eb619c28e431d98f8e4f191b4c619f3f2df41ccd8e231f7582fbf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.wanfangdata.com.cn/images/PeriodicalImages/zgsjzsyj-e/zgsjzsyj-e.jpg</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6183025/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6183025/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30233056$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Branca, Jacopo Junio Valerio</creatorcontrib><creatorcontrib>Morucci, Gabriele</creatorcontrib><creatorcontrib>Pacini, Alessandra</creatorcontrib><title>Cadmium-induced neurotoxicity: still much ado</title><title>Neural regeneration research</title><addtitle>Neural Regen Res</addtitle><description>Cadmium (Cd) is a highly toxic heavy metal that accumulates in living system and as such is currently one of the most important occupational and environmental pollutants. Cd reaches into the environment by anthropogenic mobilization and it is absorbed from tobacco consumption or ingestion of contaminated substances. Its extremely long biological half-life (approximately 20-30 years in humans) and low rate of excretion from the body cause cadmium storage predominantly in soft tissues (primarily, liver and kidneys) with a diversity of toxic effects such as nephrotoxicity, hepatotoxicity, endocrine and reproductive toxicities. Moreover, a Cd-dependent neurotoxicity has been also related to neurodegenerative diseases such as Alzheimer's and Parkinson's diseases, amyotrophic lateral sclerosis, and multiple sclerosis. At the cellular level, Cd affects cell proliferation, differentiation, apoptosis and other cellular activities. Among all these mechanisms, the Cd-dependent interference in DNA repair mechanisms as well as the generation of reactive oxygen species, seem to be the most important causes of its cellular toxicity. Nevertheless, there is still much to find out about its mechanisms of action and ways to reduce health risks. This article gives a brief review of the relevant mechanisms that it would be worth investigating in order to deep inside cadmium toxicity.</description><subject>Antioxidants</subject><subject>Binding sites</subject><subject>Cadmium</subject><subject>Cell cycle</subject><subject>Chemical properties</subject><subject>Cytotoxicity</subject><subject>Deoxyribonucleic acid</subject><subject>Disease</subject><subject>DNA</subject><subject>DNA methylation</subject><subject>Environmental aspects</subject><subject>Enzymes</subject><subject>Gene expression</subject><subject>Hazardous materials</subject><subject>Health aspects</subject><subject>Hypotheses</subject><subject>Neurotoxicity</subject><subject>Oxidative stress</subject><subject>Physiological aspects</subject><subject>Reactive oxygen species</subject><subject>Review</subject><subject>Smoking</subject><issn>1673-5374</issn><issn>1876-7958</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptUU1LAzEQDaJord49ScGjbM3nbtaDUIpfIHjRc0jzUVN2k7rZVeuvN7XaWpA5ZJh5701mHgAnCA4pguQC5QXJGCnoEJOSEroDeogXeVaUjO-m_Ld9AA5jnEHIeInJPjggEBMCWd4D2Vjq2nV15rzulNEDb7omtOHDKdcuLgexdVU1qDv1MpA6HIE9K6tojn_ePni-uX4a32UPj7f349FDphgu2kzDnBvGlTTETHJUKswNJUiX3KbEohJNqEp1SyzWliKlNDeYIFswju3Ekj64WunOu0lttDK-bWQl5o2rZbMQQTqx3fHuRUzDm8gRT7uxJHC-EniX3ko_FbPQNT59WXxO4-wzLmbCYIg4QhDShD77GdeE187EdgPHhGNEMS_gBjWVlRHO25BGq9pFJUaMUVqw8hs1_AeVQpvaqeCNdam-RYArgmpCjI2x6zURFEuXxdJGsbRRrFxOlNO_51kTfm0lX9jboKw</recordid><startdate>20181101</startdate><enddate>20181101</enddate><creator>Branca, Jacopo Junio Valerio</creator><creator>Morucci, Gabriele</creator><creator>Pacini, Alessandra</creator><general>Medknow Publications and Media Pvt. 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Cd reaches into the environment by anthropogenic mobilization and it is absorbed from tobacco consumption or ingestion of contaminated substances. Its extremely long biological half-life (approximately 20-30 years in humans) and low rate of excretion from the body cause cadmium storage predominantly in soft tissues (primarily, liver and kidneys) with a diversity of toxic effects such as nephrotoxicity, hepatotoxicity, endocrine and reproductive toxicities. Moreover, a Cd-dependent neurotoxicity has been also related to neurodegenerative diseases such as Alzheimer's and Parkinson's diseases, amyotrophic lateral sclerosis, and multiple sclerosis. At the cellular level, Cd affects cell proliferation, differentiation, apoptosis and other cellular activities. Among all these mechanisms, the Cd-dependent interference in DNA repair mechanisms as well as the generation of reactive oxygen species, seem to be the most important causes of its cellular toxicity. 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| subjects | Antioxidants Binding sites Cadmium Cell cycle Chemical properties Cytotoxicity Deoxyribonucleic acid Disease DNA DNA methylation Environmental aspects Enzymes Gene expression Hazardous materials Health aspects Hypotheses Neurotoxicity Oxidative stress Physiological aspects Reactive oxygen species Review Smoking |
| title | Cadmium-induced neurotoxicity: still much ado |
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