Loading…
C 60 Fullerene Prevents Restraint Stress-Induced Oxidative Disorders in Rat Tissues: Possible Involvement of the Nrf2/ARE-Antioxidant Pathway
The effects of C FAS (50 and 500 g/kg) supplementation, in a normal physiological state and after restraint stress exposure, on prooxidant/antioxidant balance in rat tissues were explored and compared with the effects of the known exogenous antioxidant N-acetylcysteine. Oxidative stress biomarkers...
Saved in:
Published in: | Oxidative medicine and cellular longevity 2018, Vol.2018 (1), p.2518676 |
---|---|
Main Authors: | , , , , , , , , |
Format: | Article |
Language: | English |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
cited_by | cdi_FETCH-LOGICAL-c258t-bdf325f0a0770eac11b5e62fe3c8824b6cbffb268251de46a2d9890559dd870a3 |
---|---|
cites | cdi_FETCH-LOGICAL-c258t-bdf325f0a0770eac11b5e62fe3c8824b6cbffb268251de46a2d9890559dd870a3 |
container_end_page | |
container_issue | 1 |
container_start_page | 2518676 |
container_title | Oxidative medicine and cellular longevity |
container_volume | 2018 |
creator | Gonchar, Olga O Maznychenko, Andriy V Bulgakova, Nataliya V Vereshchaka, Inna V Tomiak, Tomasz Ritter, Uwe Prylutskyy, Yuriy I Mankovska, Iryna M Kostyukov, Alexander I |
description | The effects of C
FAS (50 and 500
g/kg) supplementation, in a normal physiological state and after restraint stress exposure, on prooxidant/antioxidant balance in rat tissues were explored and compared with the effects of the known exogenous antioxidant N-acetylcysteine. Oxidative stress biomarkers (ROS, O
·
, H
O
, and lipid peroxidation) and indices of antioxidant status (MnSOD, catalase, GPx, GST,
-GCL, GR activities, and GSH level) were measured in the brain and the heart. In addition, protein expression of Nrf2 in the nuclear and cytosol fractions as well as the protein level of antiradical enzyme MnSOD and GSH-related enzymes
-GCLC, GPx, and GSTP as downstream targets of Nrf2 was evaluated by western blot analysis. Under a stress condition, C
FAS attenuates ROS generation and O
·
and H
O
releases and thus decreases lipid peroxidation as well as increases rat tissue antioxidant capacity. We have shown that C
FAS supplementation has dose-dependent and tissue-specific effects. C
FAS strengthened the antiradical defense through the upregulation of MnSOD in brain cells and maintained MnSOD protein content at the control level in the myocardium. Moreover, C
FAS enhanced the GSH level and the activity/protein expression of GSH-related enzymes. Correlation of these changes with Nrf2 protein content suggests that under stress exposure, along with other mechanisms, the Nrf2/ARE-antioxidant pathway may be involved in regulation of glutathione homeostasis. In our study, in an
model, when C
FAS (50 and 500
g/kg) was applied alone, no significant changes in Nrf2 protein expression as well as in activity/protein levels of MnSOD and GSH-related enzymes in both tissues types were observed. All these facts allow us to assume that in the
model, C
FAS affects on the brain and heart endogenous antioxidative statuses only during the oxidative stress condition. |
doi_str_mv | 10.1155/2018/2518676 |
format | article |
fullrecord | <record><control><sourceid>pubmed_cross</sourceid><recordid>TN_cdi_crossref_primary_10_1155_2018_2518676</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>30538799</sourcerecordid><originalsourceid>FETCH-LOGICAL-c258t-bdf325f0a0770eac11b5e62fe3c8824b6cbffb268251de46a2d9890559dd870a3</originalsourceid><addsrcrecordid>eNo9kNFOwjAUQBujEUTffDb9ACdtt26dbwRBSYgQxOelW29DzdhI2035CP_ZEZCne5N7cnJzELqn5IlSzoeMUDFknIo4iS9Qn6YRC0iaRpfnnZAeunHui5A4ZBG9Rr2Q8FAkadpHv2McEzxtyhIsVICXFlqovMMrcN5KU3n84S04F8wq1RSg8OLHKOlNC_jFuNoqsA6bCq-kx2vjXAPuGS9r50xeAp5VbV22sO2UuNbYbwC_W82Go9UkGFXe1AdZd1tKv_mW-1t0pWXp4O40B-hzOlmP34L54nU2Hs2DgnHhg1zpkHFNJEkSArKgNOcQMw1hIQSL8rjItc5ZLLosCqJYMpWKlHCeKiUSIsMBejx6C9t9akFnO2u20u4zSrJD1exQNTtV7fCHI75r8i2oM_yfMfwDJsFzmw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>C 60 Fullerene Prevents Restraint Stress-Induced Oxidative Disorders in Rat Tissues: Possible Involvement of the Nrf2/ARE-Antioxidant Pathway</title><source>Publicly Available Content Database (Proquest) (PQ_SDU_P3)</source><source>Open Access: Wiley-Blackwell Open Access Journals</source><creator>Gonchar, Olga O ; Maznychenko, Andriy V ; Bulgakova, Nataliya V ; Vereshchaka, Inna V ; Tomiak, Tomasz ; Ritter, Uwe ; Prylutskyy, Yuriy I ; Mankovska, Iryna M ; Kostyukov, Alexander I</creator><contributor>Saso, Luciano</contributor><creatorcontrib>Gonchar, Olga O ; Maznychenko, Andriy V ; Bulgakova, Nataliya V ; Vereshchaka, Inna V ; Tomiak, Tomasz ; Ritter, Uwe ; Prylutskyy, Yuriy I ; Mankovska, Iryna M ; Kostyukov, Alexander I ; Saso, Luciano</creatorcontrib><description>The effects of C
FAS (50 and 500
g/kg) supplementation, in a normal physiological state and after restraint stress exposure, on prooxidant/antioxidant balance in rat tissues were explored and compared with the effects of the known exogenous antioxidant N-acetylcysteine. Oxidative stress biomarkers (ROS, O
·
, H
O
, and lipid peroxidation) and indices of antioxidant status (MnSOD, catalase, GPx, GST,
-GCL, GR activities, and GSH level) were measured in the brain and the heart. In addition, protein expression of Nrf2 in the nuclear and cytosol fractions as well as the protein level of antiradical enzyme MnSOD and GSH-related enzymes
-GCLC, GPx, and GSTP as downstream targets of Nrf2 was evaluated by western blot analysis. Under a stress condition, C
FAS attenuates ROS generation and O
·
and H
O
releases and thus decreases lipid peroxidation as well as increases rat tissue antioxidant capacity. We have shown that C
FAS supplementation has dose-dependent and tissue-specific effects. C
FAS strengthened the antiradical defense through the upregulation of MnSOD in brain cells and maintained MnSOD protein content at the control level in the myocardium. Moreover, C
FAS enhanced the GSH level and the activity/protein expression of GSH-related enzymes. Correlation of these changes with Nrf2 protein content suggests that under stress exposure, along with other mechanisms, the Nrf2/ARE-antioxidant pathway may be involved in regulation of glutathione homeostasis. In our study, in an
model, when C
FAS (50 and 500
g/kg) was applied alone, no significant changes in Nrf2 protein expression as well as in activity/protein levels of MnSOD and GSH-related enzymes in both tissues types were observed. All these facts allow us to assume that in the
model, C
FAS affects on the brain and heart endogenous antioxidative statuses only during the oxidative stress condition.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2018/2518676</identifier><identifier>PMID: 30538799</identifier><language>eng</language><publisher>United States</publisher><ispartof>Oxidative medicine and cellular longevity, 2018, Vol.2018 (1), p.2518676</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c258t-bdf325f0a0770eac11b5e62fe3c8824b6cbffb268251de46a2d9890559dd870a3</citedby><cites>FETCH-LOGICAL-c258t-bdf325f0a0770eac11b5e62fe3c8824b6cbffb268251de46a2d9890559dd870a3</cites><orcidid>0000-0002-9315-4863 ; 0000-0002-9847-4137 ; 0000-0002-5109-7303 ; 0000-0003-4134-0354 ; 0000-0003-2312-4412 ; 0000-0001-9666-1839 ; 0000-0002-0621-1998 ; 0000-0001-5312-5462 ; 0000-0003-4335-3175</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30538799$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Saso, Luciano</contributor><creatorcontrib>Gonchar, Olga O</creatorcontrib><creatorcontrib>Maznychenko, Andriy V</creatorcontrib><creatorcontrib>Bulgakova, Nataliya V</creatorcontrib><creatorcontrib>Vereshchaka, Inna V</creatorcontrib><creatorcontrib>Tomiak, Tomasz</creatorcontrib><creatorcontrib>Ritter, Uwe</creatorcontrib><creatorcontrib>Prylutskyy, Yuriy I</creatorcontrib><creatorcontrib>Mankovska, Iryna M</creatorcontrib><creatorcontrib>Kostyukov, Alexander I</creatorcontrib><title>C 60 Fullerene Prevents Restraint Stress-Induced Oxidative Disorders in Rat Tissues: Possible Involvement of the Nrf2/ARE-Antioxidant Pathway</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>The effects of C
FAS (50 and 500
g/kg) supplementation, in a normal physiological state and after restraint stress exposure, on prooxidant/antioxidant balance in rat tissues were explored and compared with the effects of the known exogenous antioxidant N-acetylcysteine. Oxidative stress biomarkers (ROS, O
·
, H
O
, and lipid peroxidation) and indices of antioxidant status (MnSOD, catalase, GPx, GST,
-GCL, GR activities, and GSH level) were measured in the brain and the heart. In addition, protein expression of Nrf2 in the nuclear and cytosol fractions as well as the protein level of antiradical enzyme MnSOD and GSH-related enzymes
-GCLC, GPx, and GSTP as downstream targets of Nrf2 was evaluated by western blot analysis. Under a stress condition, C
FAS attenuates ROS generation and O
·
and H
O
releases and thus decreases lipid peroxidation as well as increases rat tissue antioxidant capacity. We have shown that C
FAS supplementation has dose-dependent and tissue-specific effects. C
FAS strengthened the antiradical defense through the upregulation of MnSOD in brain cells and maintained MnSOD protein content at the control level in the myocardium. Moreover, C
FAS enhanced the GSH level and the activity/protein expression of GSH-related enzymes. Correlation of these changes with Nrf2 protein content suggests that under stress exposure, along with other mechanisms, the Nrf2/ARE-antioxidant pathway may be involved in regulation of glutathione homeostasis. In our study, in an
model, when C
FAS (50 and 500
g/kg) was applied alone, no significant changes in Nrf2 protein expression as well as in activity/protein levels of MnSOD and GSH-related enzymes in both tissues types were observed. All these facts allow us to assume that in the
model, C
FAS affects on the brain and heart endogenous antioxidative statuses only during the oxidative stress condition.</description><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNo9kNFOwjAUQBujEUTffDb9ACdtt26dbwRBSYgQxOelW29DzdhI2035CP_ZEZCne5N7cnJzELqn5IlSzoeMUDFknIo4iS9Qn6YRC0iaRpfnnZAeunHui5A4ZBG9Rr2Q8FAkadpHv2McEzxtyhIsVICXFlqovMMrcN5KU3n84S04F8wq1RSg8OLHKOlNC_jFuNoqsA6bCq-kx2vjXAPuGS9r50xeAp5VbV22sO2UuNbYbwC_W82Go9UkGFXe1AdZd1tKv_mW-1t0pWXp4O40B-hzOlmP34L54nU2Hs2DgnHhg1zpkHFNJEkSArKgNOcQMw1hIQSL8rjItc5ZLLosCqJYMpWKlHCeKiUSIsMBejx6C9t9akFnO2u20u4zSrJD1exQNTtV7fCHI75r8i2oM_yfMfwDJsFzmw</recordid><startdate>2018</startdate><enddate>2018</enddate><creator>Gonchar, Olga O</creator><creator>Maznychenko, Andriy V</creator><creator>Bulgakova, Nataliya V</creator><creator>Vereshchaka, Inna V</creator><creator>Tomiak, Tomasz</creator><creator>Ritter, Uwe</creator><creator>Prylutskyy, Yuriy I</creator><creator>Mankovska, Iryna M</creator><creator>Kostyukov, Alexander I</creator><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><orcidid>https://orcid.org/0000-0002-9315-4863</orcidid><orcidid>https://orcid.org/0000-0002-9847-4137</orcidid><orcidid>https://orcid.org/0000-0002-5109-7303</orcidid><orcidid>https://orcid.org/0000-0003-4134-0354</orcidid><orcidid>https://orcid.org/0000-0003-2312-4412</orcidid><orcidid>https://orcid.org/0000-0001-9666-1839</orcidid><orcidid>https://orcid.org/0000-0002-0621-1998</orcidid><orcidid>https://orcid.org/0000-0001-5312-5462</orcidid><orcidid>https://orcid.org/0000-0003-4335-3175</orcidid></search><sort><creationdate>2018</creationdate><title>C 60 Fullerene Prevents Restraint Stress-Induced Oxidative Disorders in Rat Tissues: Possible Involvement of the Nrf2/ARE-Antioxidant Pathway</title><author>Gonchar, Olga O ; Maznychenko, Andriy V ; Bulgakova, Nataliya V ; Vereshchaka, Inna V ; Tomiak, Tomasz ; Ritter, Uwe ; Prylutskyy, Yuriy I ; Mankovska, Iryna M ; Kostyukov, Alexander I</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c258t-bdf325f0a0770eac11b5e62fe3c8824b6cbffb268251de46a2d9890559dd870a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gonchar, Olga O</creatorcontrib><creatorcontrib>Maznychenko, Andriy V</creatorcontrib><creatorcontrib>Bulgakova, Nataliya V</creatorcontrib><creatorcontrib>Vereshchaka, Inna V</creatorcontrib><creatorcontrib>Tomiak, Tomasz</creatorcontrib><creatorcontrib>Ritter, Uwe</creatorcontrib><creatorcontrib>Prylutskyy, Yuriy I</creatorcontrib><creatorcontrib>Mankovska, Iryna M</creatorcontrib><creatorcontrib>Kostyukov, Alexander I</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Oxidative medicine and cellular longevity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gonchar, Olga O</au><au>Maznychenko, Andriy V</au><au>Bulgakova, Nataliya V</au><au>Vereshchaka, Inna V</au><au>Tomiak, Tomasz</au><au>Ritter, Uwe</au><au>Prylutskyy, Yuriy I</au><au>Mankovska, Iryna M</au><au>Kostyukov, Alexander I</au><au>Saso, Luciano</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>C 60 Fullerene Prevents Restraint Stress-Induced Oxidative Disorders in Rat Tissues: Possible Involvement of the Nrf2/ARE-Antioxidant Pathway</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2018</date><risdate>2018</risdate><volume>2018</volume><issue>1</issue><spage>2518676</spage><pages>2518676-</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><abstract>The effects of C
FAS (50 and 500
g/kg) supplementation, in a normal physiological state and after restraint stress exposure, on prooxidant/antioxidant balance in rat tissues were explored and compared with the effects of the known exogenous antioxidant N-acetylcysteine. Oxidative stress biomarkers (ROS, O
·
, H
O
, and lipid peroxidation) and indices of antioxidant status (MnSOD, catalase, GPx, GST,
-GCL, GR activities, and GSH level) were measured in the brain and the heart. In addition, protein expression of Nrf2 in the nuclear and cytosol fractions as well as the protein level of antiradical enzyme MnSOD and GSH-related enzymes
-GCLC, GPx, and GSTP as downstream targets of Nrf2 was evaluated by western blot analysis. Under a stress condition, C
FAS attenuates ROS generation and O
·
and H
O
releases and thus decreases lipid peroxidation as well as increases rat tissue antioxidant capacity. We have shown that C
FAS supplementation has dose-dependent and tissue-specific effects. C
FAS strengthened the antiradical defense through the upregulation of MnSOD in brain cells and maintained MnSOD protein content at the control level in the myocardium. Moreover, C
FAS enhanced the GSH level and the activity/protein expression of GSH-related enzymes. Correlation of these changes with Nrf2 protein content suggests that under stress exposure, along with other mechanisms, the Nrf2/ARE-antioxidant pathway may be involved in regulation of glutathione homeostasis. In our study, in an
model, when C
FAS (50 and 500
g/kg) was applied alone, no significant changes in Nrf2 protein expression as well as in activity/protein levels of MnSOD and GSH-related enzymes in both tissues types were observed. All these facts allow us to assume that in the
model, C
FAS affects on the brain and heart endogenous antioxidative statuses only during the oxidative stress condition.</abstract><cop>United States</cop><pmid>30538799</pmid><doi>10.1155/2018/2518676</doi><orcidid>https://orcid.org/0000-0002-9315-4863</orcidid><orcidid>https://orcid.org/0000-0002-9847-4137</orcidid><orcidid>https://orcid.org/0000-0002-5109-7303</orcidid><orcidid>https://orcid.org/0000-0003-4134-0354</orcidid><orcidid>https://orcid.org/0000-0003-2312-4412</orcidid><orcidid>https://orcid.org/0000-0001-9666-1839</orcidid><orcidid>https://orcid.org/0000-0002-0621-1998</orcidid><orcidid>https://orcid.org/0000-0001-5312-5462</orcidid><orcidid>https://orcid.org/0000-0003-4335-3175</orcidid><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1942-0900 |
ispartof | Oxidative medicine and cellular longevity, 2018, Vol.2018 (1), p.2518676 |
issn | 1942-0900 1942-0994 |
language | eng |
recordid | cdi_crossref_primary_10_1155_2018_2518676 |
source | Publicly Available Content Database (Proquest) (PQ_SDU_P3); Open Access: Wiley-Blackwell Open Access Journals |
title | C 60 Fullerene Prevents Restraint Stress-Induced Oxidative Disorders in Rat Tissues: Possible Involvement of the Nrf2/ARE-Antioxidant Pathway |
url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-26T14%3A03%3A01IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-pubmed_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=C%2060%20Fullerene%20Prevents%20Restraint%20Stress-Induced%20Oxidative%20Disorders%20in%20Rat%20Tissues:%20Possible%20Involvement%20of%20the%20Nrf2/ARE-Antioxidant%20Pathway&rft.jtitle=Oxidative%20medicine%20and%20cellular%20longevity&rft.au=Gonchar,%20Olga%20O&rft.date=2018&rft.volume=2018&rft.issue=1&rft.spage=2518676&rft.pages=2518676-&rft.issn=1942-0900&rft.eissn=1942-0994&rft_id=info:doi/10.1155/2018/2518676&rft_dat=%3Cpubmed_cross%3E30538799%3C/pubmed_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c258t-bdf325f0a0770eac11b5e62fe3c8824b6cbffb268251de46a2d9890559dd870a3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_id=info:pmid/30538799&rfr_iscdi=true |