Neurotoxic effects of nickel chloride in the rainbow trout brain: Assessment of c-Fos activity, antioxidant responses, acetylcholinesterase activity, and histopathological changes
The aim of this study was to determine the biochemical, immunohistochemical, and histopathological effects of nickel chloride (Ni) in the rainbow trout brain. Fish were exposed to Ni concentrations (1 mg/L and 2 mg/L) for 21 days. At the end of the experimental period, brain tissues were taken from...
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| Veröffentlicht in: | Fish physiology and biochemistry 2015-06, Vol.41 (3), p.625-634 |
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| creator | Topal, Ahmet Atamanalp, Muhammed Oruç, Ertan Halıcı, Mesut Bünyami Şişecioğlu, Melda Erol, Hüseyin Serkan Gergit, Arzu Yılmaz, Bahar |
| description | The aim of this study was to determine the biochemical, immunohistochemical, and histopathological effects of nickel chloride (Ni) in the rainbow trout brain. Fish were exposed to Ni concentrations (1 mg/L and 2 mg/L) for 21 days. At the end of the experimental period, brain tissues were taken from all fish for c-Fos activity and histopathological examination and determination of acetylcholinesterase (AChE), superoxide dismutase (SOD), catalase (CAT) enzyme activities, lipid peroxidation (LPO), and glutathione (GSH) levels. Our results showed that Ni treatment caused a significant increase in the brain SOD activity and in LPO and GSH levels (
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| doi_str_mv | 10.1007/s10695-015-0033-1 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1768570892</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3687284881</sourcerecordid><originalsourceid>FETCH-LOGICAL-c475t-56bfd0738b6daf54205a8920d2bb2d171f3d72cb91fc2bd31cf1fd1a7348fab93</originalsourceid><addsrcrecordid>eNp1kc9u1DAQxiMEokvhAbggS1w4NOBxEjvhVlUUkCq4wNny365L1l48DrDPxQvW0RYESByske3f981ovqZ5CvQlUCpeIVA-DS2FemjXtXCv2cAgunYAPt5vNnRitAXRs5PmEeINpXQSHB42J2zgnI9cbJqfH9ySU0k_giHOe2cKkuRJDOaLm4nZzikH60iIpGwdySpEnb6TktNSiF6vr8k5okPcuVhWpWkvExJlSvgWyuGMqFhCdbe1kuxwn2Kl67Nx5TCbbZpDdFhcVuj-UlmyDVjSXpXKpOtg1DqOitcOHzcPvJrRPbmrp83nyzefLt61Vx_fvr84v2pNL4bSDlx7S0U3am6VH3pGBzXWjVimNbMgwHdWMKMn8IZp24Hx4C0o0fWjV3rqTpsXR999Tl-XOqXcBTRunlV0aUEJgo-DoNWzos__QW_SkmOdTtYogHHRQ1cpOFImJ8TsvNznsFP5IIHKNVF5TFTWROWaqISqeXbnvOids78VvyKsADsCWL_qevIfrf_regvxfrB-</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1681267413</pqid></control><display><type>article</type><title>Neurotoxic effects of nickel chloride in the rainbow trout brain: Assessment of c-Fos activity, antioxidant responses, acetylcholinesterase activity, and histopathological changes</title><source>MEDLINE</source><source>SpringerLink Journals</source><creator>Topal, Ahmet ; Atamanalp, Muhammed ; Oruç, Ertan ; Halıcı, Mesut Bünyami ; Şişecioğlu, Melda ; Erol, Hüseyin Serkan ; Gergit, Arzu ; Yılmaz, Bahar</creator><creatorcontrib>Topal, Ahmet ; Atamanalp, Muhammed ; Oruç, Ertan ; Halıcı, Mesut Bünyami ; Şişecioğlu, Melda ; Erol, Hüseyin Serkan ; Gergit, Arzu ; Yılmaz, Bahar</creatorcontrib><description>The aim of this study was to determine the biochemical, immunohistochemical, and histopathological effects of nickel chloride (Ni) in the rainbow trout brain. Fish were exposed to Ni concentrations (1 mg/L and 2 mg/L) for 21 days. At the end of the experimental period, brain tissues were taken from all fish for c-Fos activity and histopathological examination and determination of acetylcholinesterase (AChE), superoxide dismutase (SOD), catalase (CAT) enzyme activities, lipid peroxidation (LPO), and glutathione (GSH) levels. Our results showed that Ni treatment caused a significant increase in the brain SOD activity and in LPO and GSH levels (
p
< 0.05), but it significantly decreased AChE and CAT enzyme activities (
p
< 0.05). Strong induction in c-Fos was observed in some cerebral and cerebellar regions of fish exposed to Ni concentrations when compared with the control group. However, c-Fos activity was decreased in necrotic Purkinje cells. Brain tissues were characterized by demyelination and necrotic changes. These results suggested that Ni treatment causes oxidative stress, changes in c-Fos activity, and histopathological damage in the fish brain.</description><identifier>ISSN: 0920-1742</identifier><identifier>EISSN: 1573-5168</identifier><identifier>DOI: 10.1007/s10695-015-0033-1</identifier><identifier>PMID: 25666867</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Acetylcholinesterase - metabolism ; Animal Anatomy ; Animal Biochemistry ; Animal Physiology ; Animals ; Antioxidants ; Biomarkers ; Biomedical and Life Sciences ; Brain ; Brain - drug effects ; Brain - metabolism ; Brain - pathology ; Catalase - metabolism ; Chloride ; Enzymatic activity ; Enzymes ; Fish ; Fisheries ; Freshwater & Marine Ecology ; Glutathione - metabolism ; Heavy metals ; Histology ; Immunohistochemistry - veterinary ; Industrial development ; Life Sciences ; Lipid Peroxidation - physiology ; Morphology ; Neurotoxicity ; Neurotoxins - toxicity ; Nickel ; Nickel - toxicity ; Oncorhynchus mykiss ; Oncorhynchus mykiss - metabolism ; Oxidative stress ; Oxidative Stress - drug effects ; Peroxidation ; Pollutants ; Proto-Oncogene Proteins c-fos - metabolism ; Superoxide Dismutase - metabolism ; Toxicity ; Trout ; Zoology</subject><ispartof>Fish physiology and biochemistry, 2015-06, Vol.41 (3), p.625-634</ispartof><rights>Springer Science+Business Media Dordrecht 2015</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c475t-56bfd0738b6daf54205a8920d2bb2d171f3d72cb91fc2bd31cf1fd1a7348fab93</citedby><cites>FETCH-LOGICAL-c475t-56bfd0738b6daf54205a8920d2bb2d171f3d72cb91fc2bd31cf1fd1a7348fab93</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/s10695-015-0033-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10695-015-0033-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25666867$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Topal, Ahmet</creatorcontrib><creatorcontrib>Atamanalp, Muhammed</creatorcontrib><creatorcontrib>Oruç, Ertan</creatorcontrib><creatorcontrib>Halıcı, Mesut Bünyami</creatorcontrib><creatorcontrib>Şişecioğlu, Melda</creatorcontrib><creatorcontrib>Erol, Hüseyin Serkan</creatorcontrib><creatorcontrib>Gergit, Arzu</creatorcontrib><creatorcontrib>Yılmaz, Bahar</creatorcontrib><title>Neurotoxic effects of nickel chloride in the rainbow trout brain: Assessment of c-Fos activity, antioxidant responses, acetylcholinesterase activity, and histopathological changes</title><title>Fish physiology and biochemistry</title><addtitle>Fish Physiol Biochem</addtitle><addtitle>Fish Physiol Biochem</addtitle><description>The aim of this study was to determine the biochemical, immunohistochemical, and histopathological effects of nickel chloride (Ni) in the rainbow trout brain. Fish were exposed to Ni concentrations (1 mg/L and 2 mg/L) for 21 days. At the end of the experimental period, brain tissues were taken from all fish for c-Fos activity and histopathological examination and determination of acetylcholinesterase (AChE), superoxide dismutase (SOD), catalase (CAT) enzyme activities, lipid peroxidation (LPO), and glutathione (GSH) levels. Our results showed that Ni treatment caused a significant increase in the brain SOD activity and in LPO and GSH levels (
p
< 0.05), but it significantly decreased AChE and CAT enzyme activities (
p
< 0.05). Strong induction in c-Fos was observed in some cerebral and cerebellar regions of fish exposed to Ni concentrations when compared with the control group. However, c-Fos activity was decreased in necrotic Purkinje cells. Brain tissues were characterized by demyelination and necrotic changes. These results suggested that Ni treatment causes oxidative stress, changes in c-Fos activity, and histopathological damage in the fish brain.</description><subject>Acetylcholinesterase - metabolism</subject><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Animal Physiology</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Biomarkers</subject><subject>Biomedical and Life Sciences</subject><subject>Brain</subject><subject>Brain - drug effects</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Catalase - metabolism</subject><subject>Chloride</subject><subject>Enzymatic activity</subject><subject>Enzymes</subject><subject>Fish</subject><subject>Fisheries</subject><subject>Freshwater & Marine Ecology</subject><subject>Glutathione - metabolism</subject><subject>Heavy metals</subject><subject>Histology</subject><subject>Immunohistochemistry - veterinary</subject><subject>Industrial development</subject><subject>Life Sciences</subject><subject>Lipid Peroxidation - physiology</subject><subject>Morphology</subject><subject>Neurotoxicity</subject><subject>Neurotoxins - toxicity</subject><subject>Nickel</subject><subject>Nickel - toxicity</subject><subject>Oncorhynchus mykiss</subject><subject>Oncorhynchus mykiss - metabolism</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Peroxidation</subject><subject>Pollutants</subject><subject>Proto-Oncogene Proteins c-fos - metabolism</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Toxicity</subject><subject>Trout</subject><subject>Zoology</subject><issn>0920-1742</issn><issn>1573-5168</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kc9u1DAQxiMEokvhAbggS1w4NOBxEjvhVlUUkCq4wNny365L1l48DrDPxQvW0RYESByske3f981ovqZ5CvQlUCpeIVA-DS2FemjXtXCv2cAgunYAPt5vNnRitAXRs5PmEeINpXQSHB42J2zgnI9cbJqfH9ySU0k_giHOe2cKkuRJDOaLm4nZzikH60iIpGwdySpEnb6TktNSiF6vr8k5okPcuVhWpWkvExJlSvgWyuGMqFhCdbe1kuxwn2Kl67Nx5TCbbZpDdFhcVuj-UlmyDVjSXpXKpOtg1DqOitcOHzcPvJrRPbmrp83nyzefLt61Vx_fvr84v2pNL4bSDlx7S0U3am6VH3pGBzXWjVimNbMgwHdWMKMn8IZp24Hx4C0o0fWjV3rqTpsXR999Tl-XOqXcBTRunlV0aUEJgo-DoNWzos__QW_SkmOdTtYogHHRQ1cpOFImJ8TsvNznsFP5IIHKNVF5TFTWROWaqISqeXbnvOids78VvyKsADsCWL_qevIfrf_regvxfrB-</recordid><startdate>20150601</startdate><enddate>20150601</enddate><creator>Topal, Ahmet</creator><creator>Atamanalp, 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effects of nickel chloride in the rainbow trout brain: Assessment of c-Fos activity, antioxidant responses, acetylcholinesterase activity, and histopathological changes</title><author>Topal, Ahmet ; Atamanalp, Muhammed ; Oruç, Ertan ; Halıcı, Mesut Bünyami ; Şişecioğlu, Melda ; Erol, Hüseyin Serkan ; Gergit, Arzu ; Yılmaz, Bahar</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c475t-56bfd0738b6daf54205a8920d2bb2d171f3d72cb91fc2bd31cf1fd1a7348fab93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Acetylcholinesterase - metabolism</topic><topic>Animal Anatomy</topic><topic>Animal Biochemistry</topic><topic>Animal Physiology</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Biomarkers</topic><topic>Biomedical and Life Sciences</topic><topic>Brain</topic><topic>Brain - drug effects</topic><topic>Brain - metabolism</topic><topic>Brain - 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Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Topal, Ahmet</au><au>Atamanalp, Muhammed</au><au>Oruç, Ertan</au><au>Halıcı, Mesut Bünyami</au><au>Şişecioğlu, Melda</au><au>Erol, Hüseyin Serkan</au><au>Gergit, Arzu</au><au>Yılmaz, Bahar</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neurotoxic effects of nickel chloride in the rainbow trout brain: Assessment of c-Fos activity, antioxidant responses, acetylcholinesterase activity, and histopathological changes</atitle><jtitle>Fish physiology and biochemistry</jtitle><stitle>Fish Physiol Biochem</stitle><addtitle>Fish Physiol Biochem</addtitle><date>2015-06-01</date><risdate>2015</risdate><volume>41</volume><issue>3</issue><spage>625</spage><epage>634</epage><pages>625-634</pages><issn>0920-1742</issn><eissn>1573-5168</eissn><abstract>The aim of this study was to determine the biochemical, immunohistochemical, and histopathological effects of nickel chloride (Ni) in the rainbow trout brain. Fish were exposed to Ni concentrations (1 mg/L and 2 mg/L) for 21 days. At the end of the experimental period, brain tissues were taken from all fish for c-Fos activity and histopathological examination and determination of acetylcholinesterase (AChE), superoxide dismutase (SOD), catalase (CAT) enzyme activities, lipid peroxidation (LPO), and glutathione (GSH) levels. Our results showed that Ni treatment caused a significant increase in the brain SOD activity and in LPO and GSH levels (
p
< 0.05), but it significantly decreased AChE and CAT enzyme activities (
p
< 0.05). Strong induction in c-Fos was observed in some cerebral and cerebellar regions of fish exposed to Ni concentrations when compared with the control group. However, c-Fos activity was decreased in necrotic Purkinje cells. Brain tissues were characterized by demyelination and necrotic changes. These results suggested that Ni treatment causes oxidative stress, changes in c-Fos activity, and histopathological damage in the fish brain.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>25666867</pmid><doi>10.1007/s10695-015-0033-1</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0920-1742 |
| ispartof | Fish physiology and biochemistry, 2015-06, Vol.41 (3), p.625-634 |
| issn | 0920-1742 1573-5168 |
| language | eng |
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| source | MEDLINE; SpringerLink Journals |
| subjects | Acetylcholinesterase - metabolism Animal Anatomy Animal Biochemistry Animal Physiology Animals Antioxidants Biomarkers Biomedical and Life Sciences Brain Brain - drug effects Brain - metabolism Brain - pathology Catalase - metabolism Chloride Enzymatic activity Enzymes Fish Fisheries Freshwater & Marine Ecology Glutathione - metabolism Heavy metals Histology Immunohistochemistry - veterinary Industrial development Life Sciences Lipid Peroxidation - physiology Morphology Neurotoxicity Neurotoxins - toxicity Nickel Nickel - toxicity Oncorhynchus mykiss Oncorhynchus mykiss - metabolism Oxidative stress Oxidative Stress - drug effects Peroxidation Pollutants Proto-Oncogene Proteins c-fos - metabolism Superoxide Dismutase - metabolism Toxicity Trout Zoology |
| title | Neurotoxic effects of nickel chloride in the rainbow trout brain: Assessment of c-Fos activity, antioxidant responses, acetylcholinesterase activity, and histopathological changes |
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