Impairment of cell and plasma redox state in subjects professionally exposed to chromium
Background Chromium (Cr) is widely used in chemical, tannery, building, and metal industries. More recently, it has been demonstrated that Cr induces oxidative stress in mouse brain. Nevertheless very few data exist on in vivo oxidative damage in humans exposed to Cr. Methods Changes in antioxidant...
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| Veröffentlicht in: | American journal of industrial medicine 2004-08, Vol.46 (2), p.120-125 |
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| creator | Mattia, Giancarlo De Bravi, Maria Cristina Laurenti, Oriana Luca, Orietta De Palmeri, Alessandro Sabatucci, Antonio Mendico, Gino Ghiselli, Andrea |
| description | Background
Chromium (Cr) is widely used in chemical, tannery, building, and metal industries. More recently, it has been demonstrated that Cr induces oxidative stress in mouse brain. Nevertheless very few data exist on in vivo oxidative damage in humans exposed to Cr.
Methods
Changes in antioxidant parameters both in plasma (acid ascorbic redox state and total antioxidant capacity) and in red blood cells (glutathione (GSH) redox state) of 40 subjects (age 37.65 ± 7.46; M/F 20/20) professionally exposed to Cr who were recruited from metal, chemistry, and building industries were evaluated. We also evaluated the levels of lipoperoxidation (thiobarbituric acid‐reactive material, TBA‐RM) and thiol levels in plasma to assess the extent of oxidative stress state. To evaluate Cr exposure rate, we measured urinary‐chromium (U‐Cr) by an electrothermic atomization‐atomic absorption spectrometry (ETA‐AAS) method.
Results
In this study, we found that Cr exposure induced a decrease both in GSH (P |
| doi_str_mv | 10.1002/ajim.20044 |
| format | Article |
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Chromium (Cr) is widely used in chemical, tannery, building, and metal industries. More recently, it has been demonstrated that Cr induces oxidative stress in mouse brain. Nevertheless very few data exist on in vivo oxidative damage in humans exposed to Cr.
Methods
Changes in antioxidant parameters both in plasma (acid ascorbic redox state and total antioxidant capacity) and in red blood cells (glutathione (GSH) redox state) of 40 subjects (age 37.65 ± 7.46; M/F 20/20) professionally exposed to Cr who were recruited from metal, chemistry, and building industries were evaluated. We also evaluated the levels of lipoperoxidation (thiobarbituric acid‐reactive material, TBA‐RM) and thiol levels in plasma to assess the extent of oxidative stress state. To evaluate Cr exposure rate, we measured urinary‐chromium (U‐Cr) by an electrothermic atomization‐atomic absorption spectrometry (ETA‐AAS) method.
Results
In this study, we found that Cr exposure induced a decrease both in GSH (P < 0.0005) and GSH/oxidized glutathione (GSSG) ratio (P < 0.0001) in red blood cells from workers with respect to control subjects. Furthermore, we also demonstrated a significant decrease of plasma acid ascorbic levels (45.7 ± 14.9 vs. 53.5 ± 16.5 μmol/L; P < 0.05) and in total plasma antioxidant capacity (1,126.3 ± 212.2 vs. 1,266.9 ± 207.8 μmol/L; P < 0.05) in subjects exposed to Cr. No difference was found with regard to TBA‐RM and thiol levels.
Conclusions
This study demonstrated that in humans, an oxidative stress occurs for Cr exposures as low as those considered safe. This oxidative stress appears to be able to affect intracellular and plasmatic antioxidant defense. Am. J. Ind. Med. 46:120–125, 2004. © 2004 Wiley‐Liss, Inc.</description><identifier>ISSN: 0271-3586</identifier><identifier>EISSN: 1097-0274</identifier><identifier>DOI: 10.1002/ajim.20044</identifier><identifier>PMID: 15273963</identifier><identifier>CODEN: AJIMD8</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Adult ; ascorbic acid ; Ascorbic Acid - blood ; Biological and medical sciences ; Chemical and industrial products toxicology. Toxic occupational diseases ; Chromium ; Erythrocytes - chemistry ; Erythrocytes - metabolism ; Female ; glutathione ; Glutathione - blood ; Humans ; Lipid Peroxidation ; Male ; Medical sciences ; Metals and various inorganic compounds ; Middle Aged ; Occupational Exposure ; Oxidation-Reduction ; oxidative stress ; Oxidative Stress - physiology ; reactive oxygen species ; Toxicology</subject><ispartof>American journal of industrial medicine, 2004-08, Vol.46 (2), p.120-125</ispartof><rights>Copyright © 2004 Wiley‐Liss, Inc.</rights><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4244-66e9f4a2aeca9afaa03467118710cfdbdc16df572d293a7df11c7e3aaad84b23</citedby><cites>FETCH-LOGICAL-c4244-66e9f4a2aeca9afaa03467118710cfdbdc16df572d293a7df11c7e3aaad84b23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fajim.20044$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fajim.20044$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15980708$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15273963$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mattia, Giancarlo De</creatorcontrib><creatorcontrib>Bravi, Maria Cristina</creatorcontrib><creatorcontrib>Laurenti, Oriana</creatorcontrib><creatorcontrib>Luca, Orietta De</creatorcontrib><creatorcontrib>Palmeri, Alessandro</creatorcontrib><creatorcontrib>Sabatucci, Antonio</creatorcontrib><creatorcontrib>Mendico, Gino</creatorcontrib><creatorcontrib>Ghiselli, Andrea</creatorcontrib><title>Impairment of cell and plasma redox state in subjects professionally exposed to chromium</title><title>American journal of industrial medicine</title><addtitle>Am. J. Ind. Med</addtitle><description>Background
Chromium (Cr) is widely used in chemical, tannery, building, and metal industries. More recently, it has been demonstrated that Cr induces oxidative stress in mouse brain. Nevertheless very few data exist on in vivo oxidative damage in humans exposed to Cr.
Methods
Changes in antioxidant parameters both in plasma (acid ascorbic redox state and total antioxidant capacity) and in red blood cells (glutathione (GSH) redox state) of 40 subjects (age 37.65 ± 7.46; M/F 20/20) professionally exposed to Cr who were recruited from metal, chemistry, and building industries were evaluated. We also evaluated the levels of lipoperoxidation (thiobarbituric acid‐reactive material, TBA‐RM) and thiol levels in plasma to assess the extent of oxidative stress state. To evaluate Cr exposure rate, we measured urinary‐chromium (U‐Cr) by an electrothermic atomization‐atomic absorption spectrometry (ETA‐AAS) method.
Results
In this study, we found that Cr exposure induced a decrease both in GSH (P < 0.0005) and GSH/oxidized glutathione (GSSG) ratio (P < 0.0001) in red blood cells from workers with respect to control subjects. Furthermore, we also demonstrated a significant decrease of plasma acid ascorbic levels (45.7 ± 14.9 vs. 53.5 ± 16.5 μmol/L; P < 0.05) and in total plasma antioxidant capacity (1,126.3 ± 212.2 vs. 1,266.9 ± 207.8 μmol/L; P < 0.05) in subjects exposed to Cr. No difference was found with regard to TBA‐RM and thiol levels.
Conclusions
This study demonstrated that in humans, an oxidative stress occurs for Cr exposures as low as those considered safe. This oxidative stress appears to be able to affect intracellular and plasmatic antioxidant defense. Am. J. Ind. Med. 46:120–125, 2004. © 2004 Wiley‐Liss, Inc.</description><subject>Adult</subject><subject>ascorbic acid</subject><subject>Ascorbic Acid - blood</subject><subject>Biological and medical sciences</subject><subject>Chemical and industrial products toxicology. Toxic occupational diseases</subject><subject>Chromium</subject><subject>Erythrocytes - chemistry</subject><subject>Erythrocytes - metabolism</subject><subject>Female</subject><subject>glutathione</subject><subject>Glutathione - blood</subject><subject>Humans</subject><subject>Lipid Peroxidation</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metals and various inorganic compounds</subject><subject>Middle Aged</subject><subject>Occupational Exposure</subject><subject>Oxidation-Reduction</subject><subject>oxidative stress</subject><subject>Oxidative Stress - physiology</subject><subject>reactive oxygen species</subject><subject>Toxicology</subject><issn>0271-3586</issn><issn>1097-0274</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp90Mtu00AUBuARAtFQ2PAAaDawqOQyN3vsZaloSQkgoUrtbnQyFzHB9rhzbJG8PQ4JlxWrs_nO7SfkJWfnnDHxFjaxOxeMKfWILDhrdMGEVo_JYi68kGVdnZBniBvGOFeVekpOeCm0bCq5IPfLboCYO9-PNAVqfdtS6B0dWsAOaPYubSmOMHoae4rTeuPtiHTIKXjEmHpo2x312yGhd3RM1H7LqYtT95w8CdCif3Gsp-T26v3t5Ydi9eV6eXmxKqwSShVV5ZugQIC30EAAYFJVmvNac2aDWzvLKxdKLZxoJGgXOLfaSwBwtVoLeUreHMbOFz1MHkfTRdx_Ab1PExquddmoupnh2QHanBCzD2bIsYO8M5yZfYxmH6P5FeOMXx2nTuvOu7_0mNsMXh8BoIU2ZOhtxH9cUzPN6tnxg_sRW7_7z0pzcbP89Ht5ceiJOPrtnx7I302lpS7N3edr8_HrStzcvbs3pfwJ362bCA</recordid><startdate>200408</startdate><enddate>200408</enddate><creator>Mattia, Giancarlo De</creator><creator>Bravi, Maria Cristina</creator><creator>Laurenti, Oriana</creator><creator>Luca, Orietta De</creator><creator>Palmeri, Alessandro</creator><creator>Sabatucci, Antonio</creator><creator>Mendico, Gino</creator><creator>Ghiselli, Andrea</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</general><scope>BSCLL</scope><scope>IQODW</scope><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>7U7</scope><scope>C1K</scope></search><sort><creationdate>200408</creationdate><title>Impairment of cell and plasma redox state in subjects professionally exposed to chromium</title><author>Mattia, Giancarlo De ; Bravi, Maria Cristina ; Laurenti, Oriana ; Luca, Orietta De ; Palmeri, Alessandro ; Sabatucci, Antonio ; Mendico, Gino ; Ghiselli, Andrea</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4244-66e9f4a2aeca9afaa03467118710cfdbdc16df572d293a7df11c7e3aaad84b23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adult</topic><topic>ascorbic acid</topic><topic>Ascorbic Acid - blood</topic><topic>Biological and medical sciences</topic><topic>Chemical and industrial products toxicology. Toxic occupational diseases</topic><topic>Chromium</topic><topic>Erythrocytes - chemistry</topic><topic>Erythrocytes - metabolism</topic><topic>Female</topic><topic>glutathione</topic><topic>Glutathione - blood</topic><topic>Humans</topic><topic>Lipid Peroxidation</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metals and various inorganic compounds</topic><topic>Middle Aged</topic><topic>Occupational Exposure</topic><topic>Oxidation-Reduction</topic><topic>oxidative stress</topic><topic>Oxidative Stress - physiology</topic><topic>reactive oxygen species</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mattia, Giancarlo De</creatorcontrib><creatorcontrib>Bravi, Maria Cristina</creatorcontrib><creatorcontrib>Laurenti, Oriana</creatorcontrib><creatorcontrib>Luca, Orietta De</creatorcontrib><creatorcontrib>Palmeri, Alessandro</creatorcontrib><creatorcontrib>Sabatucci, Antonio</creatorcontrib><creatorcontrib>Mendico, Gino</creatorcontrib><creatorcontrib>Ghiselli, Andrea</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>American journal of industrial medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mattia, Giancarlo De</au><au>Bravi, Maria Cristina</au><au>Laurenti, Oriana</au><au>Luca, Orietta De</au><au>Palmeri, Alessandro</au><au>Sabatucci, Antonio</au><au>Mendico, Gino</au><au>Ghiselli, Andrea</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impairment of cell and plasma redox state in subjects professionally exposed to chromium</atitle><jtitle>American journal of industrial medicine</jtitle><addtitle>Am. J. Ind. Med</addtitle><date>2004-08</date><risdate>2004</risdate><volume>46</volume><issue>2</issue><spage>120</spage><epage>125</epage><pages>120-125</pages><issn>0271-3586</issn><eissn>1097-0274</eissn><coden>AJIMD8</coden><abstract>Background
Chromium (Cr) is widely used in chemical, tannery, building, and metal industries. More recently, it has been demonstrated that Cr induces oxidative stress in mouse brain. Nevertheless very few data exist on in vivo oxidative damage in humans exposed to Cr.
Methods
Changes in antioxidant parameters both in plasma (acid ascorbic redox state and total antioxidant capacity) and in red blood cells (glutathione (GSH) redox state) of 40 subjects (age 37.65 ± 7.46; M/F 20/20) professionally exposed to Cr who were recruited from metal, chemistry, and building industries were evaluated. We also evaluated the levels of lipoperoxidation (thiobarbituric acid‐reactive material, TBA‐RM) and thiol levels in plasma to assess the extent of oxidative stress state. To evaluate Cr exposure rate, we measured urinary‐chromium (U‐Cr) by an electrothermic atomization‐atomic absorption spectrometry (ETA‐AAS) method.
Results
In this study, we found that Cr exposure induced a decrease both in GSH (P < 0.0005) and GSH/oxidized glutathione (GSSG) ratio (P < 0.0001) in red blood cells from workers with respect to control subjects. Furthermore, we also demonstrated a significant decrease of plasma acid ascorbic levels (45.7 ± 14.9 vs. 53.5 ± 16.5 μmol/L; P < 0.05) and in total plasma antioxidant capacity (1,126.3 ± 212.2 vs. 1,266.9 ± 207.8 μmol/L; P < 0.05) in subjects exposed to Cr. No difference was found with regard to TBA‐RM and thiol levels.
Conclusions
This study demonstrated that in humans, an oxidative stress occurs for Cr exposures as low as those considered safe. This oxidative stress appears to be able to affect intracellular and plasmatic antioxidant defense. Am. J. Ind. Med. 46:120–125, 2004. © 2004 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>15273963</pmid><doi>10.1002/ajim.20044</doi><tpages>6</tpages></addata></record> |
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| subjects | Adult ascorbic acid Ascorbic Acid - blood Biological and medical sciences Chemical and industrial products toxicology. Toxic occupational diseases Chromium Erythrocytes - chemistry Erythrocytes - metabolism Female glutathione Glutathione - blood Humans Lipid Peroxidation Male Medical sciences Metals and various inorganic compounds Middle Aged Occupational Exposure Oxidation-Reduction oxidative stress Oxidative Stress - physiology reactive oxygen species Toxicology |
| title | Impairment of cell and plasma redox state in subjects professionally exposed to chromium |
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