Neuronal Apoptosis and Imbalance of Neurotransmitters Induced by Acetamiprid in Rats

Recent toxicological studies have demonstrated that exposure to organochlorine pesticides is susceptible to produce various alterations in brain cell which significantly contribute to a loss in neurobehavioral skills and disturbance of neuronal function. Acetamipride (AC) is belonging to this organo...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Toxicology and environmental health sciences 2019-12, Vol.11 (4), p.305-311
Hauptverfasser: Gasmi, Salim, Chafaa, Smail, Lakroun, Zhora, Rouabhi, Rachid, Touahria, Chouaib, Kebieche, Mohamed, Soulimani, Rachid
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 311
container_issue 4
container_start_page 305
container_title Toxicology and environmental health sciences
container_volume 11
creator Gasmi, Salim
Chafaa, Smail
Lakroun, Zhora
Rouabhi, Rachid
Touahria, Chouaib
Kebieche, Mohamed
Soulimani, Rachid
description Recent toxicological studies have demonstrated that exposure to organochlorine pesticides is susceptible to produce various alterations in brain cell which significantly contribute to a loss in neurobehavioral skills and disturbance of neuronal function. Acetamipride (AC) is belonging to this organochlorines family and it is considered less harmful by toxicovigilance systems and practices in Algeria. The aim of this work was mainly to evaluate the impact of this pesticide on the brain cell integrity and function in Acetamiprid-treated rats at the dose of 3.14 mg/kg (1/60 Lethal Dose) daily during 3 months. Several indicators of neuronal apoptosis and function have been rated, in addition to classical labyrinth and Maze tests monitoring to evaluate learning and memorization abilities in rats exposed to this neonicotinoid. The results of this study have shown significant enhancing of cytochrome-c(p
doi_str_mv 10.1007/s13530-019-0417-1
format Article
fullrecord <record><control><sourceid>proquest_hal_p</sourceid><recordid>TN_cdi_hal_primary_oai_HAL_hal_02983658v1</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2343273118</sourcerecordid><originalsourceid>FETCH-LOGICAL-c350t-f6fbe740803c74d63ad91a548adf5cc7e7ef1fa4d80f5e2c60414feef38bc43b3</originalsourceid><addsrcrecordid>eNp1kE1LxDAQhoMouOj-AG8BTx6i-Wza47Kou7AoyHoOaZpol36ZpML-e1MrenIuMwzPvMz7AnBF8C3BWN4FwgTDCJMCYU4kIidgQSljSMqcn6YZY4EKKeg5WIZwwKl4RklWLMD-yY6-73QDV0M_xD7UAequgtu21I3ujIW9g99M9LoLbR2j9QFuu2o0toLlEa6MjbqtB19XsO7gi47hEpw53QS7_OkX4PXhfr_eoN3z43a92iHDBI7IZa60kuMcMyN5lTFdFUQLnuvKCWOkldYRp3mVYycsNVkyx521juWl4axkF-Bm1n3XjUoPtNofVa9rtVnt1LTDtMhZJvJPktjrmR18_zHaENWhH30yHhRlnFHJCMkTRWbK-D4Eb92vLMFqylrNWauUtZqyVpMynW9CYrs36_-U_z_6Av5igQw</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2343273118</pqid></control><display><type>article</type><title>Neuronal Apoptosis and Imbalance of Neurotransmitters Induced by Acetamiprid in Rats</title><source>SpringerNature Journals</source><creator>Gasmi, Salim ; Chafaa, Smail ; Lakroun, Zhora ; Rouabhi, Rachid ; Touahria, Chouaib ; Kebieche, Mohamed ; Soulimani, Rachid</creator><creatorcontrib>Gasmi, Salim ; Chafaa, Smail ; Lakroun, Zhora ; Rouabhi, Rachid ; Touahria, Chouaib ; Kebieche, Mohamed ; Soulimani, Rachid</creatorcontrib><description><![CDATA[Recent toxicological studies have demonstrated that exposure to organochlorine pesticides is susceptible to produce various alterations in brain cell which significantly contribute to a loss in neurobehavioral skills and disturbance of neuronal function. Acetamipride (AC) is belonging to this organochlorines family and it is considered less harmful by toxicovigilance systems and practices in Algeria. The aim of this work was mainly to evaluate the impact of this pesticide on the brain cell integrity and function in Acetamiprid-treated rats at the dose of 3.14 mg/kg (1/60 Lethal Dose) daily during 3 months. Several indicators of neuronal apoptosis and function have been rated, in addition to classical labyrinth and Maze tests monitoring to evaluate learning and memorization abilities in rats exposed to this neonicotinoid. The results of this study have shown significant enhancing of cytochrome-c(p<0.01) and Caspase-3(p<0.001) activities in brain lysates of treated group that is correlated with induction of apoptosis. At the same time, assessment of neurotrans-mitters brain cells has recorded a significant increase (p<0.01) in adrenaline rate and a significant decrease in cerebral level of dopamine (p< 0.01), serotonin (p<0.001) and Acetylcholin esterase in the same group comparing to control. Furthermore, neurobehavioral study has shown a strong correlation between the unbalance observed in neurotransmitters homeostasis and the significant (p<0.01) loss of learning, memorization and locomotive potential as demonstrated by the increase in arrival time(S) (10.33±3.14) versus (3.33±2.05) in control. In conclusion, exposition of the rats to Acetamiprid generates apoptosis which is induced by releasing of mitochondrial Cytochrome-c in cell cytosol and alters neurotransmitters rates that could reduce the potential of learning and memorization in the rats.]]></description><identifier>ISSN: 2005-9752</identifier><identifier>EISSN: 2233-7784</identifier><identifier>DOI: 10.1007/s13530-019-0417-1</identifier><language>eng</language><publisher>Seoul: Korean Society of Environmental Risk Assessment and Health Science</publisher><subject>Apoptosis ; Biomedical and Life Sciences ; Biomedicine ; Brain ; Caspase-3 ; Correlation analysis ; Cytochrome ; Cytochrome c ; Cytochromes ; Cytosol ; Dopamine ; Environmental Health ; Epinephrine ; Esterase ; Evaluation ; Exposure ; Homeostasis ; Labyrinth ; Learning ; Lethal dose ; Life Sciences ; Lysates ; Maze learning ; Memory ; Mitochondria ; Neurotransmitters ; Organic compounds ; Organochlorine compounds ; Organochlorine pesticides ; Original Article ; Pesticides ; Pharmacology/Toxicology ; Serotonin ; Toxicity testing ; Toxicology</subject><ispartof>Toxicology and environmental health sciences, 2019-12, Vol.11 (4), p.305-311</ispartof><rights>The Korean Society of Environmental Risk Assessment and Health Science and Springer 2019</rights><rights>2019© The Korean Society of Environmental Risk Assessment and Health Science and Springer 2019</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c350t-f6fbe740803c74d63ad91a548adf5cc7e7ef1fa4d80f5e2c60414feef38bc43b3</citedby><cites>FETCH-LOGICAL-c350t-f6fbe740803c74d63ad91a548adf5cc7e7ef1fa4d80f5e2c60414feef38bc43b3</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/s13530-019-0417-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s13530-019-0417-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,780,784,885,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://hal.inrae.fr/hal-02983658$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Gasmi, Salim</creatorcontrib><creatorcontrib>Chafaa, Smail</creatorcontrib><creatorcontrib>Lakroun, Zhora</creatorcontrib><creatorcontrib>Rouabhi, Rachid</creatorcontrib><creatorcontrib>Touahria, Chouaib</creatorcontrib><creatorcontrib>Kebieche, Mohamed</creatorcontrib><creatorcontrib>Soulimani, Rachid</creatorcontrib><title>Neuronal Apoptosis and Imbalance of Neurotransmitters Induced by Acetamiprid in Rats</title><title>Toxicology and environmental health sciences</title><addtitle>Toxicol. Environ. Health Sci</addtitle><description><![CDATA[Recent toxicological studies have demonstrated that exposure to organochlorine pesticides is susceptible to produce various alterations in brain cell which significantly contribute to a loss in neurobehavioral skills and disturbance of neuronal function. Acetamipride (AC) is belonging to this organochlorines family and it is considered less harmful by toxicovigilance systems and practices in Algeria. The aim of this work was mainly to evaluate the impact of this pesticide on the brain cell integrity and function in Acetamiprid-treated rats at the dose of 3.14 mg/kg (1/60 Lethal Dose) daily during 3 months. Several indicators of neuronal apoptosis and function have been rated, in addition to classical labyrinth and Maze tests monitoring to evaluate learning and memorization abilities in rats exposed to this neonicotinoid. The results of this study have shown significant enhancing of cytochrome-c(p<0.01) and Caspase-3(p<0.001) activities in brain lysates of treated group that is correlated with induction of apoptosis. At the same time, assessment of neurotrans-mitters brain cells has recorded a significant increase (p<0.01) in adrenaline rate and a significant decrease in cerebral level of dopamine (p< 0.01), serotonin (p<0.001) and Acetylcholin esterase in the same group comparing to control. Furthermore, neurobehavioral study has shown a strong correlation between the unbalance observed in neurotransmitters homeostasis and the significant (p<0.01) loss of learning, memorization and locomotive potential as demonstrated by the increase in arrival time(S) (10.33±3.14) versus (3.33±2.05) in control. In conclusion, exposition of the rats to Acetamiprid generates apoptosis which is induced by releasing of mitochondrial Cytochrome-c in cell cytosol and alters neurotransmitters rates that could reduce the potential of learning and memorization in the rats.]]></description><subject>Apoptosis</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain</subject><subject>Caspase-3</subject><subject>Correlation analysis</subject><subject>Cytochrome</subject><subject>Cytochrome c</subject><subject>Cytochromes</subject><subject>Cytosol</subject><subject>Dopamine</subject><subject>Environmental Health</subject><subject>Epinephrine</subject><subject>Esterase</subject><subject>Evaluation</subject><subject>Exposure</subject><subject>Homeostasis</subject><subject>Labyrinth</subject><subject>Learning</subject><subject>Lethal dose</subject><subject>Life Sciences</subject><subject>Lysates</subject><subject>Maze learning</subject><subject>Memory</subject><subject>Mitochondria</subject><subject>Neurotransmitters</subject><subject>Organic compounds</subject><subject>Organochlorine compounds</subject><subject>Organochlorine pesticides</subject><subject>Original Article</subject><subject>Pesticides</subject><subject>Pharmacology/Toxicology</subject><subject>Serotonin</subject><subject>Toxicity testing</subject><subject>Toxicology</subject><issn>2005-9752</issn><issn>2233-7784</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNp1kE1LxDAQhoMouOj-AG8BTx6i-Wza47Kou7AoyHoOaZpol36ZpML-e1MrenIuMwzPvMz7AnBF8C3BWN4FwgTDCJMCYU4kIidgQSljSMqcn6YZY4EKKeg5WIZwwKl4RklWLMD-yY6-73QDV0M_xD7UAequgtu21I3ujIW9g99M9LoLbR2j9QFuu2o0toLlEa6MjbqtB19XsO7gi47hEpw53QS7_OkX4PXhfr_eoN3z43a92iHDBI7IZa60kuMcMyN5lTFdFUQLnuvKCWOkldYRp3mVYycsNVkyx521juWl4axkF-Bm1n3XjUoPtNofVa9rtVnt1LTDtMhZJvJPktjrmR18_zHaENWhH30yHhRlnFHJCMkTRWbK-D4Eb92vLMFqylrNWauUtZqyVpMynW9CYrs36_-U_z_6Av5igQw</recordid><startdate>20191201</startdate><enddate>20191201</enddate><creator>Gasmi, Salim</creator><creator>Chafaa, Smail</creator><creator>Lakroun, Zhora</creator><creator>Rouabhi, Rachid</creator><creator>Touahria, Chouaib</creator><creator>Kebieche, Mohamed</creator><creator>Soulimani, Rachid</creator><general>Korean Society of Environmental Risk Assessment and Health Science</general><general>Springer Nature B.V</general><scope>AAYXX</scope><scope>CITATION</scope><scope>1XC</scope></search><sort><creationdate>20191201</creationdate><title>Neuronal Apoptosis and Imbalance of Neurotransmitters Induced by Acetamiprid in Rats</title><author>Gasmi, Salim ; Chafaa, Smail ; Lakroun, Zhora ; Rouabhi, Rachid ; Touahria, Chouaib ; Kebieche, Mohamed ; Soulimani, Rachid</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c350t-f6fbe740803c74d63ad91a548adf5cc7e7ef1fa4d80f5e2c60414feef38bc43b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Apoptosis</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain</topic><topic>Caspase-3</topic><topic>Correlation analysis</topic><topic>Cytochrome</topic><topic>Cytochrome c</topic><topic>Cytochromes</topic><topic>Cytosol</topic><topic>Dopamine</topic><topic>Environmental Health</topic><topic>Epinephrine</topic><topic>Esterase</topic><topic>Evaluation</topic><topic>Exposure</topic><topic>Homeostasis</topic><topic>Labyrinth</topic><topic>Learning</topic><topic>Lethal dose</topic><topic>Life Sciences</topic><topic>Lysates</topic><topic>Maze learning</topic><topic>Memory</topic><topic>Mitochondria</topic><topic>Neurotransmitters</topic><topic>Organic compounds</topic><topic>Organochlorine compounds</topic><topic>Organochlorine pesticides</topic><topic>Original Article</topic><topic>Pesticides</topic><topic>Pharmacology/Toxicology</topic><topic>Serotonin</topic><topic>Toxicity testing</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gasmi, Salim</creatorcontrib><creatorcontrib>Chafaa, Smail</creatorcontrib><creatorcontrib>Lakroun, Zhora</creatorcontrib><creatorcontrib>Rouabhi, Rachid</creatorcontrib><creatorcontrib>Touahria, Chouaib</creatorcontrib><creatorcontrib>Kebieche, Mohamed</creatorcontrib><creatorcontrib>Soulimani, Rachid</creatorcontrib><collection>CrossRef</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Toxicology and environmental health sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gasmi, Salim</au><au>Chafaa, Smail</au><au>Lakroun, Zhora</au><au>Rouabhi, Rachid</au><au>Touahria, Chouaib</au><au>Kebieche, Mohamed</au><au>Soulimani, Rachid</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuronal Apoptosis and Imbalance of Neurotransmitters Induced by Acetamiprid in Rats</atitle><jtitle>Toxicology and environmental health sciences</jtitle><stitle>Toxicol. Environ. Health Sci</stitle><date>2019-12-01</date><risdate>2019</risdate><volume>11</volume><issue>4</issue><spage>305</spage><epage>311</epage><pages>305-311</pages><issn>2005-9752</issn><eissn>2233-7784</eissn><abstract><![CDATA[Recent toxicological studies have demonstrated that exposure to organochlorine pesticides is susceptible to produce various alterations in brain cell which significantly contribute to a loss in neurobehavioral skills and disturbance of neuronal function. Acetamipride (AC) is belonging to this organochlorines family and it is considered less harmful by toxicovigilance systems and practices in Algeria. The aim of this work was mainly to evaluate the impact of this pesticide on the brain cell integrity and function in Acetamiprid-treated rats at the dose of 3.14 mg/kg (1/60 Lethal Dose) daily during 3 months. Several indicators of neuronal apoptosis and function have been rated, in addition to classical labyrinth and Maze tests monitoring to evaluate learning and memorization abilities in rats exposed to this neonicotinoid. The results of this study have shown significant enhancing of cytochrome-c(p<0.01) and Caspase-3(p<0.001) activities in brain lysates of treated group that is correlated with induction of apoptosis. At the same time, assessment of neurotrans-mitters brain cells has recorded a significant increase (p<0.01) in adrenaline rate and a significant decrease in cerebral level of dopamine (p< 0.01), serotonin (p<0.001) and Acetylcholin esterase in the same group comparing to control. Furthermore, neurobehavioral study has shown a strong correlation between the unbalance observed in neurotransmitters homeostasis and the significant (p<0.01) loss of learning, memorization and locomotive potential as demonstrated by the increase in arrival time(S) (10.33±3.14) versus (3.33±2.05) in control. In conclusion, exposition of the rats to Acetamiprid generates apoptosis which is induced by releasing of mitochondrial Cytochrome-c in cell cytosol and alters neurotransmitters rates that could reduce the potential of learning and memorization in the rats.]]></abstract><cop>Seoul</cop><pub>Korean Society of Environmental Risk Assessment and Health Science</pub><doi>10.1007/s13530-019-0417-1</doi><tpages>7</tpages></addata></record>
fulltext fulltext
identifier ISSN: 2005-9752
ispartof Toxicology and environmental health sciences, 2019-12, Vol.11 (4), p.305-311
issn 2005-9752
2233-7784
language eng
recordid cdi_hal_primary_oai_HAL_hal_02983658v1
source SpringerNature Journals
subjects Apoptosis
Biomedical and Life Sciences
Biomedicine
Brain
Caspase-3
Correlation analysis
Cytochrome
Cytochrome c
Cytochromes
Cytosol
Dopamine
Environmental Health
Epinephrine
Esterase
Evaluation
Exposure
Homeostasis
Labyrinth
Learning
Lethal dose
Life Sciences
Lysates
Maze learning
Memory
Mitochondria
Neurotransmitters
Organic compounds
Organochlorine compounds
Organochlorine pesticides
Original Article
Pesticides
Pharmacology/Toxicology
Serotonin
Toxicity testing
Toxicology
title Neuronal Apoptosis and Imbalance of Neurotransmitters Induced by Acetamiprid in Rats
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-26T06%3A31%3A47IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_hal_p&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Neuronal%20Apoptosis%20and%20Imbalance%20of%20Neurotransmitters%20Induced%20by%20Acetamiprid%20in%20Rats&rft.jtitle=Toxicology%20and%20environmental%20health%20sciences&rft.au=Gasmi,%20Salim&rft.date=2019-12-01&rft.volume=11&rft.issue=4&rft.spage=305&rft.epage=311&rft.pages=305-311&rft.issn=2005-9752&rft.eissn=2233-7784&rft_id=info:doi/10.1007/s13530-019-0417-1&rft_dat=%3Cproquest_hal_p%3E2343273118%3C/proquest_hal_p%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2343273118&rft_id=info:pmid/&rfr_iscdi=true