Sodium nitrite potentiates renal oxidative stress and injury in hemoglobin exposed guinea pigs
Abstract Methemoglobin-forming drugs, such as sodium nitrite (NaNO2 ), may exacerbate oxidative toxicity under certain chronic or acute hemolytic settings. In this study, we evaluated markers of renal oxidative stress and injury in guinea pigs exposed to extracellular hemoglobin (Hb) followed by NaN...
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| Veröffentlicht in: | Toxicology (Amsterdam) 2015-07, Vol.333, p.89-99 |
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| creator | Baek, Jin Hyen Zhang, Xiaoyuan Williams, Matthew C Hicks, Wayne Buehler, Paul W D’Agnillo, Felice |
| description | Abstract Methemoglobin-forming drugs, such as sodium nitrite (NaNO2 ), may exacerbate oxidative toxicity under certain chronic or acute hemolytic settings. In this study, we evaluated markers of renal oxidative stress and injury in guinea pigs exposed to extracellular hemoglobin (Hb) followed by NaNO2 at doses sufficient to simulate clinically relevant acute methemoglobinemia. NaNO2 induced rapid and extensive oxidation of plasma Hb in this model. This was accompanied by increased renal expression of the oxidative response effectors nuclear factor erythroid 2-derived-factor 2 (Nrf-2) and heme oxygenase-1 (HO-1), elevated non-heme iron deposition, lipid peroxidation, interstitial inflammatory cell activation, increased expression of tubular injury markers kidney injury-1 marker (KIM-1) and liver-fatty acid binding protein (L-FABP), podocyte injury, and cell death. Importantly, these indicators of renal oxidative stress and injury were minimal or absent following infusion of Hb or NaNO2 alone. Together, these results suggest that the exposure to NaNO2 in settings associated with increased extracellular Hb may potentiate acute renal toxicity via processes that are independent of NaNO2 induced erythrocyte methemoglobinemia. |
| doi_str_mv | 10.1016/j.tox.2015.04.007 |
| format | Article |
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In this study, we evaluated markers of renal oxidative stress and injury in guinea pigs exposed to extracellular hemoglobin (Hb) followed by NaNO2 at doses sufficient to simulate clinically relevant acute methemoglobinemia. NaNO2 induced rapid and extensive oxidation of plasma Hb in this model. This was accompanied by increased renal expression of the oxidative response effectors nuclear factor erythroid 2-derived-factor 2 (Nrf-2) and heme oxygenase-1 (HO-1), elevated non-heme iron deposition, lipid peroxidation, interstitial inflammatory cell activation, increased expression of tubular injury markers kidney injury-1 marker (KIM-1) and liver-fatty acid binding protein (L-FABP), podocyte injury, and cell death. Importantly, these indicators of renal oxidative stress and injury were minimal or absent following infusion of Hb or NaNO2 alone. Together, these results suggest that the exposure to NaNO2 in settings associated with increased extracellular Hb may potentiate acute renal toxicity via processes that are independent of NaNO2 induced erythrocyte methemoglobinemia.</description><identifier>ISSN: 0300-483X</identifier><identifier>EISSN: 1879-3185</identifier><identifier>DOI: 10.1016/j.tox.2015.04.007</identifier><identifier>PMID: 25891524</identifier><language>eng</language><publisher>Ireland: Elsevier B.V</publisher><subject>Acute Kidney Injury - blood ; Acute Kidney Injury - chemically induced ; Acute Kidney Injury - pathology ; Animals ; Biomarkers ; Biomarkers - metabolism ; Cell Death - drug effects ; Dose-Response Relationship, Drug ; Drug Synergism ; Emergency ; Exposure ; Fatty Acid-Binding Proteins - metabolism ; Guinea Pigs ; Heme ; Heme Oxygenase-1 - metabolism ; Hemoglobin ; Hemoglobins - administration & dosage ; Hemoglobins - toxicity ; Infusions, Intravenous ; Injuries ; Kidney ; Kidney - drug effects ; Kidney - metabolism ; Kidney - pathology ; Lipid Peroxidation - drug effects ; Male ; Markers ; Methemoglobin - metabolism ; Methemoglobinemia - blood ; Methemoglobinemia - chemically induced ; Methemoglobinemia - pathology ; Nanostructure ; NF-E2-Related Factor 2 - metabolism ; Nitrates - administration & dosage ; Nitrates - toxicity ; Nitrite ; Oxidation-Reduction ; Oxidative stress ; Oxidative Stress - drug effects ; Sodium nitrite ; Stresses ; Time Factors ; Toxicity</subject><ispartof>Toxicology (Amsterdam), 2015-07, Vol.333, p.89-99</ispartof><rights>2015</rights><rights>Published by Elsevier Ireland Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-da4aae4bde173c0c5e5227bb6db9569f82e69a4d29b555e0313415d38f25d0523</citedby><cites>FETCH-LOGICAL-c474t-da4aae4bde173c0c5e5227bb6db9569f82e69a4d29b555e0313415d38f25d0523</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.tox.2015.04.007$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25891524$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Baek, Jin Hyen</creatorcontrib><creatorcontrib>Zhang, Xiaoyuan</creatorcontrib><creatorcontrib>Williams, Matthew C</creatorcontrib><creatorcontrib>Hicks, Wayne</creatorcontrib><creatorcontrib>Buehler, Paul W</creatorcontrib><creatorcontrib>D’Agnillo, Felice</creatorcontrib><title>Sodium nitrite potentiates renal oxidative stress and injury in hemoglobin exposed guinea pigs</title><title>Toxicology (Amsterdam)</title><addtitle>Toxicology</addtitle><description>Abstract Methemoglobin-forming drugs, such as sodium nitrite (NaNO2 ), may exacerbate oxidative toxicity under certain chronic or acute hemolytic settings. In this study, we evaluated markers of renal oxidative stress and injury in guinea pigs exposed to extracellular hemoglobin (Hb) followed by NaNO2 at doses sufficient to simulate clinically relevant acute methemoglobinemia. NaNO2 induced rapid and extensive oxidation of plasma Hb in this model. This was accompanied by increased renal expression of the oxidative response effectors nuclear factor erythroid 2-derived-factor 2 (Nrf-2) and heme oxygenase-1 (HO-1), elevated non-heme iron deposition, lipid peroxidation, interstitial inflammatory cell activation, increased expression of tubular injury markers kidney injury-1 marker (KIM-1) and liver-fatty acid binding protein (L-FABP), podocyte injury, and cell death. Importantly, these indicators of renal oxidative stress and injury were minimal or absent following infusion of Hb or NaNO2 alone. Together, these results suggest that the exposure to NaNO2 in settings associated with increased extracellular Hb may potentiate acute renal toxicity via processes that are independent of NaNO2 induced erythrocyte methemoglobinemia.</description><subject>Acute Kidney Injury - blood</subject><subject>Acute Kidney Injury - chemically induced</subject><subject>Acute Kidney Injury - pathology</subject><subject>Animals</subject><subject>Biomarkers</subject><subject>Biomarkers - metabolism</subject><subject>Cell Death - drug effects</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug Synergism</subject><subject>Emergency</subject><subject>Exposure</subject><subject>Fatty Acid-Binding Proteins - metabolism</subject><subject>Guinea Pigs</subject><subject>Heme</subject><subject>Heme Oxygenase-1 - metabolism</subject><subject>Hemoglobin</subject><subject>Hemoglobins - administration & dosage</subject><subject>Hemoglobins - toxicity</subject><subject>Infusions, Intravenous</subject><subject>Injuries</subject><subject>Kidney</subject><subject>Kidney - drug effects</subject><subject>Kidney - metabolism</subject><subject>Kidney - pathology</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Male</subject><subject>Markers</subject><subject>Methemoglobin - metabolism</subject><subject>Methemoglobinemia - blood</subject><subject>Methemoglobinemia - chemically induced</subject><subject>Methemoglobinemia - pathology</subject><subject>Nanostructure</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>Nitrates - administration & dosage</subject><subject>Nitrates - toxicity</subject><subject>Nitrite</subject><subject>Oxidation-Reduction</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Sodium nitrite</subject><subject>Stresses</subject><subject>Time Factors</subject><subject>Toxicity</subject><issn>0300-483X</issn><issn>1879-3185</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkk2LFDEQhoMo7rj6A7xIjl66rXxNdyMIsqwfsOBhFTwZ0knNmLa70ybpZebfm2FWDx7EU-XwvC-kniLkOYOaAdu-GuocDjUHpmqQNUDzgGxY23SVYK16SDYgACrZiq8X5ElKAwBwIbePyQVXbccUlxvy7TY4v0509jn6jHQJGefsTcZEI85mpOHgncn-DmnKEVOiZnbUz8Maj2XQ7ziF_Rj68sTDEhI6ul_9jIYufp-ekkc7MyZ8dj8vyZd315-vPlQ3n95_vHp7U1nZyFw5I41B2TtkjbBgFSrOm77fur5T227Xctx2Rjre9UopBMGEZMqJdseVA8XFJXl57l1i-LliynryyeI4mhnDmjRroGuk5Jz9D8pk2zVCFZSdURtDShF3eol-MvGoGeiTAT3oYkCfDGiQuhgomRf39Ws_ofuT-L3yArw-A1j2cecx6mQ9zhadj2izdsH_s_7NX2k7-tlbM_7AI6YhrLFIK7_QiWvQt6cTOF0AU8V-0yrxCxNorIg</recordid><startdate>20150703</startdate><enddate>20150703</enddate><creator>Baek, Jin Hyen</creator><creator>Zhang, Xiaoyuan</creator><creator>Williams, Matthew C</creator><creator>Hicks, Wayne</creator><creator>Buehler, Paul W</creator><creator>D’Agnillo, Felice</creator><general>Elsevier B.V</general><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>7ST</scope><scope>7U7</scope><scope>C1K</scope><scope>SOI</scope><scope>8FD</scope><scope>FR3</scope><scope>KR7</scope></search><sort><creationdate>20150703</creationdate><title>Sodium nitrite potentiates renal oxidative stress and injury in hemoglobin exposed guinea pigs</title><author>Baek, Jin Hyen ; Zhang, Xiaoyuan ; Williams, Matthew C ; Hicks, Wayne ; Buehler, Paul W ; D’Agnillo, Felice</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-da4aae4bde173c0c5e5227bb6db9569f82e69a4d29b555e0313415d38f25d0523</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Acute Kidney Injury - blood</topic><topic>Acute Kidney Injury - chemically induced</topic><topic>Acute Kidney Injury - pathology</topic><topic>Animals</topic><topic>Biomarkers</topic><topic>Biomarkers - metabolism</topic><topic>Cell Death - drug effects</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug Synergism</topic><topic>Emergency</topic><topic>Exposure</topic><topic>Fatty Acid-Binding Proteins - metabolism</topic><topic>Guinea Pigs</topic><topic>Heme</topic><topic>Heme Oxygenase-1 - metabolism</topic><topic>Hemoglobin</topic><topic>Hemoglobins - administration & dosage</topic><topic>Hemoglobins - toxicity</topic><topic>Infusions, Intravenous</topic><topic>Injuries</topic><topic>Kidney</topic><topic>Kidney - drug effects</topic><topic>Kidney - metabolism</topic><topic>Kidney - pathology</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Male</topic><topic>Markers</topic><topic>Methemoglobin - metabolism</topic><topic>Methemoglobinemia - blood</topic><topic>Methemoglobinemia - chemically induced</topic><topic>Methemoglobinemia - pathology</topic><topic>Nanostructure</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>Nitrates - administration & dosage</topic><topic>Nitrates - toxicity</topic><topic>Nitrite</topic><topic>Oxidation-Reduction</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Sodium nitrite</topic><topic>Stresses</topic><topic>Time Factors</topic><topic>Toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Baek, Jin Hyen</creatorcontrib><creatorcontrib>Zhang, Xiaoyuan</creatorcontrib><creatorcontrib>Williams, Matthew C</creatorcontrib><creatorcontrib>Hicks, Wayne</creatorcontrib><creatorcontrib>Buehler, Paul W</creatorcontrib><creatorcontrib>D’Agnillo, Felice</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Environment Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Environment Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Civil Engineering Abstracts</collection><jtitle>Toxicology (Amsterdam)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Baek, Jin Hyen</au><au>Zhang, Xiaoyuan</au><au>Williams, Matthew C</au><au>Hicks, Wayne</au><au>Buehler, Paul W</au><au>D’Agnillo, Felice</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sodium nitrite potentiates renal oxidative stress and injury in hemoglobin exposed guinea pigs</atitle><jtitle>Toxicology (Amsterdam)</jtitle><addtitle>Toxicology</addtitle><date>2015-07-03</date><risdate>2015</risdate><volume>333</volume><spage>89</spage><epage>99</epage><pages>89-99</pages><issn>0300-483X</issn><eissn>1879-3185</eissn><abstract>Abstract Methemoglobin-forming drugs, such as sodium nitrite (NaNO2 ), may exacerbate oxidative toxicity under certain chronic or acute hemolytic settings. In this study, we evaluated markers of renal oxidative stress and injury in guinea pigs exposed to extracellular hemoglobin (Hb) followed by NaNO2 at doses sufficient to simulate clinically relevant acute methemoglobinemia. NaNO2 induced rapid and extensive oxidation of plasma Hb in this model. This was accompanied by increased renal expression of the oxidative response effectors nuclear factor erythroid 2-derived-factor 2 (Nrf-2) and heme oxygenase-1 (HO-1), elevated non-heme iron deposition, lipid peroxidation, interstitial inflammatory cell activation, increased expression of tubular injury markers kidney injury-1 marker (KIM-1) and liver-fatty acid binding protein (L-FABP), podocyte injury, and cell death. Importantly, these indicators of renal oxidative stress and injury were minimal or absent following infusion of Hb or NaNO2 alone. Together, these results suggest that the exposure to NaNO2 in settings associated with increased extracellular Hb may potentiate acute renal toxicity via processes that are independent of NaNO2 induced erythrocyte methemoglobinemia.</abstract><cop>Ireland</cop><pub>Elsevier B.V</pub><pmid>25891524</pmid><doi>10.1016/j.tox.2015.04.007</doi><tpages>11</tpages></addata></record> |
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| subjects | Acute Kidney Injury - blood Acute Kidney Injury - chemically induced Acute Kidney Injury - pathology Animals Biomarkers Biomarkers - metabolism Cell Death - drug effects Dose-Response Relationship, Drug Drug Synergism Emergency Exposure Fatty Acid-Binding Proteins - metabolism Guinea Pigs Heme Heme Oxygenase-1 - metabolism Hemoglobin Hemoglobins - administration & dosage Hemoglobins - toxicity Infusions, Intravenous Injuries Kidney Kidney - drug effects Kidney - metabolism Kidney - pathology Lipid Peroxidation - drug effects Male Markers Methemoglobin - metabolism Methemoglobinemia - blood Methemoglobinemia - chemically induced Methemoglobinemia - pathology Nanostructure NF-E2-Related Factor 2 - metabolism Nitrates - administration & dosage Nitrates - toxicity Nitrite Oxidation-Reduction Oxidative stress Oxidative Stress - drug effects Sodium nitrite Stresses Time Factors Toxicity |
| title | Sodium nitrite potentiates renal oxidative stress and injury in hemoglobin exposed guinea pigs |
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