Differential metabolism of 4-hydroxynonenal in liver, lung and brain of mice and rats
The lipid peroxidation end-product 4-hydroxynonenal (4-HNE) is generated in tissues during oxidative stress. As a reactive aldehyde, it forms Michael adducts with nucleophiles, a process that disrupts cellular functioning. Liver, lung and brain are highly sensitive to xenobiotic-induced oxidative st...
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description | The lipid peroxidation end-product 4-hydroxynonenal (4-HNE) is generated in tissues during oxidative stress. As a reactive aldehyde, it forms Michael adducts with nucleophiles, a process that disrupts cellular functioning. Liver, lung and brain are highly sensitive to xenobiotic-induced oxidative stress and readily generate 4-HNE. In the present studies, we compared 4-HNE metabolism in these tissues, a process that protects against tissue injury. 4-HNE was degraded slowly in total homogenates and S9 fractions of mouse liver, lung and brain. In liver, but not lung or brain, NAD(P)+ and NAD(P)H markedly stimulated 4-HNE metabolism. Similar results were observed in rat S9 fractions from these tissues. In liver, lung and brain S9 fractions, 4-HNE formed protein adducts. When NADH was used to stimulate 4-HNE metabolism, the formation of protein adducts was suppressed in liver, but not lung or brain. In both mouse and rat tissues, 4-HNE was also metabolized by glutathione S-transferases. The greatest activity was noted in livers of mice and in lungs of rats; relatively low glutathione S-transferase activity was detected in brain. In mouse hepatocytes, 4-HNE was rapidly taken up and metabolized. Simultaneously, 4-HNE-protein adducts were formed, suggesting that 4-HNE metabolism in intact cells does not prevent protein modifications. These data demonstrate that, in contrast to liver, lung and brain have a limited capacity to metabolize 4-HNE. The persistence of 4-HNE in these tissues may increase the likelihood of tissue injury during oxidative stress.
[Display omitted]
•Lipid peroxidation generates 4-hydroxynonenal, a highly reactive aldehyde.•Rodent liver, but not lung or brain, is efficient in degrading 4-hydroxynonenal.•4-hydroxynonenal persists in tissues with low metabolism, causing tissue damage. |
doi_str_mv | 10.1016/j.taap.2014.04.026 |
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[Display omitted]
•Lipid peroxidation generates 4-hydroxynonenal, a highly reactive aldehyde.•Rodent liver, but not lung or brain, is efficient in degrading 4-hydroxynonenal.•4-hydroxynonenal persists in tissues with low metabolism, causing tissue damage.</description><identifier>ISSN: 0041-008X</identifier><identifier>EISSN: 1096-0333</identifier><identifier>DOI: 10.1016/j.taap.2014.04.026</identifier><identifier>PMID: 24832492</identifier><identifier>CODEN: TXAPA9</identifier><language>eng</language><publisher>Amsterdam: Elsevier Inc</publisher><subject>4-Hydroxynonenal ; 60 APPLIED LIFE SCIENCES ; ALCOHOL DEHYDROGENASE ; Aldehydes - antagonists & inhibitors ; Aldehydes - metabolism ; ANIMAL TISSUES ; Animals ; Antibodies, Blocking - pharmacology ; Biological and medical sciences ; Blotting, Western ; BRAIN ; Brain - drug effects ; Brain - enzymology ; Brain - metabolism ; Enzyme Inhibitors - pharmacology ; GLUTATHIONE ; Glutathione Transferase - antagonists & inhibitors ; Glutathione Transferase - metabolism ; Hepatocytes - drug effects ; Hepatocytes - metabolism ; HOMOGENATES ; INJURIES ; Kinetics ; Lipid peroxidation ; LIPIDS ; LIVER ; Liver - drug effects ; Liver - enzymology ; Liver - metabolism ; LIVER CELLS ; Lung - drug effects ; Lung - enzymology ; Lung - metabolism ; LUNGS ; Male ; Medical sciences ; METABOLISM ; MICE ; Mice, Inbred C57BL ; NAD ; Neurotoxicity ; OXIDATION ; Pulmonary toxicity ; RATS ; Rats, Long-Evans ; Reactive oxygen species ; Species Specificity ; STRESSES ; Subcellular Fractions - enzymology ; Subcellular Fractions - metabolism ; TOXICITY ; Toxicology ; TRANSFERASES</subject><ispartof>Toxicology and applied pharmacology, 2014-08, Vol.279 (1), p.43-52</ispartof><rights>2014 Elsevier Inc.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2014 Elsevier Inc. All rights reserved.</rights><rights>2014 Elsevier Inc. All rights reserved. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c612t-b8f91a7a5ac006f3a837b80d5b7937dd5301bdc0b1d5d0736713057433e357c03</citedby><cites>FETCH-LOGICAL-c612t-b8f91a7a5ac006f3a837b80d5b7937dd5301bdc0b1d5d0736713057433e357c03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0041008X14001823$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=28599236$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24832492$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/22439803$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Zheng, Ruijin</creatorcontrib><creatorcontrib>Dragomir, Ana-Cristina</creatorcontrib><creatorcontrib>Mishin, Vladimir</creatorcontrib><creatorcontrib>Richardson, Jason R.</creatorcontrib><creatorcontrib>Heck, Diane E.</creatorcontrib><creatorcontrib>Laskin, Debra L.</creatorcontrib><creatorcontrib>Laskin, Jeffrey D.</creatorcontrib><title>Differential metabolism of 4-hydroxynonenal in liver, lung and brain of mice and rats</title><title>Toxicology and applied pharmacology</title><addtitle>Toxicol Appl Pharmacol</addtitle><description>The lipid peroxidation end-product 4-hydroxynonenal (4-HNE) is generated in tissues during oxidative stress. As a reactive aldehyde, it forms Michael adducts with nucleophiles, a process that disrupts cellular functioning. Liver, lung and brain are highly sensitive to xenobiotic-induced oxidative stress and readily generate 4-HNE. In the present studies, we compared 4-HNE metabolism in these tissues, a process that protects against tissue injury. 4-HNE was degraded slowly in total homogenates and S9 fractions of mouse liver, lung and brain. In liver, but not lung or brain, NAD(P)+ and NAD(P)H markedly stimulated 4-HNE metabolism. Similar results were observed in rat S9 fractions from these tissues. In liver, lung and brain S9 fractions, 4-HNE formed protein adducts. When NADH was used to stimulate 4-HNE metabolism, the formation of protein adducts was suppressed in liver, but not lung or brain. In both mouse and rat tissues, 4-HNE was also metabolized by glutathione S-transferases. The greatest activity was noted in livers of mice and in lungs of rats; relatively low glutathione S-transferase activity was detected in brain. In mouse hepatocytes, 4-HNE was rapidly taken up and metabolized. Simultaneously, 4-HNE-protein adducts were formed, suggesting that 4-HNE metabolism in intact cells does not prevent protein modifications. These data demonstrate that, in contrast to liver, lung and brain have a limited capacity to metabolize 4-HNE. The persistence of 4-HNE in these tissues may increase the likelihood of tissue injury during oxidative stress.
[Display omitted]
•Lipid peroxidation generates 4-hydroxynonenal, a highly reactive aldehyde.•Rodent liver, but not lung or brain, is efficient in degrading 4-hydroxynonenal.•4-hydroxynonenal persists in tissues with low metabolism, causing tissue damage.</description><subject>4-Hydroxynonenal</subject><subject>60 APPLIED LIFE SCIENCES</subject><subject>ALCOHOL DEHYDROGENASE</subject><subject>Aldehydes - antagonists & inhibitors</subject><subject>Aldehydes - metabolism</subject><subject>ANIMAL TISSUES</subject><subject>Animals</subject><subject>Antibodies, Blocking - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>BRAIN</subject><subject>Brain - drug effects</subject><subject>Brain - enzymology</subject><subject>Brain - metabolism</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>GLUTATHIONE</subject><subject>Glutathione Transferase - antagonists & inhibitors</subject><subject>Glutathione Transferase - metabolism</subject><subject>Hepatocytes - drug effects</subject><subject>Hepatocytes - metabolism</subject><subject>HOMOGENATES</subject><subject>INJURIES</subject><subject>Kinetics</subject><subject>Lipid peroxidation</subject><subject>LIPIDS</subject><subject>LIVER</subject><subject>Liver - drug effects</subject><subject>Liver - enzymology</subject><subject>Liver - metabolism</subject><subject>LIVER CELLS</subject><subject>Lung - drug effects</subject><subject>Lung - enzymology</subject><subject>Lung - metabolism</subject><subject>LUNGS</subject><subject>Male</subject><subject>Medical sciences</subject><subject>METABOLISM</subject><subject>MICE</subject><subject>Mice, Inbred C57BL</subject><subject>NAD</subject><subject>Neurotoxicity</subject><subject>OXIDATION</subject><subject>Pulmonary toxicity</subject><subject>RATS</subject><subject>Rats, Long-Evans</subject><subject>Reactive oxygen species</subject><subject>Species Specificity</subject><subject>STRESSES</subject><subject>Subcellular Fractions - enzymology</subject><subject>Subcellular Fractions - metabolism</subject><subject>TOXICITY</subject><subject>Toxicology</subject><subject>TRANSFERASES</subject><issn>0041-008X</issn><issn>1096-0333</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU2LFDEQhoMo7uzoH_AgDSJ4sMfKRyfdsAjLrl-w4MUFbyGdpHcydCdjkhl2_r1pZ1z1YigIVD15U28VQi8wrDBg_m6zykptVwQwW0EJwh-hBYaO10ApfYwWAAzXAO33M3Se0gYAOsbwU3RGWEsJ68gC3V67YbDR-uzUWE02qz6MLk1VGCpWrw8mhvuDD976Una-Gt3exrfVuPN3lfKm6qMq2QJPTttfmahyeoaeDGpM9vnpXqLbjx--XX2ub75--nJ1eVNrjkmu-3bosBKqURqAD1S1VPQtmKYXHRXGNBRwbzT02DQGBOUCU2gEo9TSRmigS_T-qLvd9ZM1utiIapTb6CYVDzIoJ_-teLeWd2EvGeYCeFcEXh0FQspOJu2y1WsdvLc6S0IY7doyyyV6c_omhh87m7KcXNJ2HJW3YZck5kR0ohxeUHJEdQwpRTs8NINBzluTGzlvTc5bk1CCzI9e_m3j4cnvNRXg9QlQSatxiMprl_5wbdMVaha6OHK2DH3vbJwtWa-tcXF2ZIL7Xx8_AdOptUI</recordid><startdate>20140815</startdate><enddate>20140815</enddate><creator>Zheng, Ruijin</creator><creator>Dragomir, Ana-Cristina</creator><creator>Mishin, Vladimir</creator><creator>Richardson, Jason R.</creator><creator>Heck, Diane E.</creator><creator>Laskin, Debra L.</creator><creator>Laskin, Jeffrey D.</creator><general>Elsevier Inc</general><general>Elsevier</general><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><scope>OTOTI</scope><scope>5PM</scope></search><sort><creationdate>20140815</creationdate><title>Differential metabolism of 4-hydroxynonenal in liver, lung and brain of mice and rats</title><author>Zheng, Ruijin ; Dragomir, Ana-Cristina ; Mishin, Vladimir ; Richardson, Jason R. ; Heck, Diane E. ; Laskin, Debra L. ; Laskin, Jeffrey D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c612t-b8f91a7a5ac006f3a837b80d5b7937dd5301bdc0b1d5d0736713057433e357c03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>4-Hydroxynonenal</topic><topic>60 APPLIED LIFE SCIENCES</topic><topic>ALCOHOL DEHYDROGENASE</topic><topic>Aldehydes - antagonists & inhibitors</topic><topic>Aldehydes - metabolism</topic><topic>ANIMAL TISSUES</topic><topic>Animals</topic><topic>Antibodies, Blocking - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>BRAIN</topic><topic>Brain - drug effects</topic><topic>Brain - enzymology</topic><topic>Brain - metabolism</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>GLUTATHIONE</topic><topic>Glutathione Transferase - antagonists & inhibitors</topic><topic>Glutathione Transferase - metabolism</topic><topic>Hepatocytes - drug effects</topic><topic>Hepatocytes - metabolism</topic><topic>HOMOGENATES</topic><topic>INJURIES</topic><topic>Kinetics</topic><topic>Lipid peroxidation</topic><topic>LIPIDS</topic><topic>LIVER</topic><topic>Liver - drug effects</topic><topic>Liver - enzymology</topic><topic>Liver - metabolism</topic><topic>LIVER CELLS</topic><topic>Lung - drug effects</topic><topic>Lung - enzymology</topic><topic>Lung - metabolism</topic><topic>LUNGS</topic><topic>Male</topic><topic>Medical sciences</topic><topic>METABOLISM</topic><topic>MICE</topic><topic>Mice, Inbred C57BL</topic><topic>NAD</topic><topic>Neurotoxicity</topic><topic>OXIDATION</topic><topic>Pulmonary toxicity</topic><topic>RATS</topic><topic>Rats, Long-Evans</topic><topic>Reactive oxygen species</topic><topic>Species Specificity</topic><topic>STRESSES</topic><topic>Subcellular Fractions - enzymology</topic><topic>Subcellular Fractions - metabolism</topic><topic>TOXICITY</topic><topic>Toxicology</topic><topic>TRANSFERASES</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zheng, Ruijin</creatorcontrib><creatorcontrib>Dragomir, Ana-Cristina</creatorcontrib><creatorcontrib>Mishin, Vladimir</creatorcontrib><creatorcontrib>Richardson, Jason R.</creatorcontrib><creatorcontrib>Heck, Diane E.</creatorcontrib><creatorcontrib>Laskin, Debra L.</creatorcontrib><creatorcontrib>Laskin, Jeffrey D.</creatorcontrib><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><collection>OSTI.GOV</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Toxicology and applied pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zheng, Ruijin</au><au>Dragomir, Ana-Cristina</au><au>Mishin, Vladimir</au><au>Richardson, Jason R.</au><au>Heck, Diane E.</au><au>Laskin, Debra L.</au><au>Laskin, Jeffrey D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differential metabolism of 4-hydroxynonenal in liver, lung and brain of mice and rats</atitle><jtitle>Toxicology and applied pharmacology</jtitle><addtitle>Toxicol Appl Pharmacol</addtitle><date>2014-08-15</date><risdate>2014</risdate><volume>279</volume><issue>1</issue><spage>43</spage><epage>52</epage><pages>43-52</pages><issn>0041-008X</issn><eissn>1096-0333</eissn><coden>TXAPA9</coden><abstract>The lipid peroxidation end-product 4-hydroxynonenal (4-HNE) is generated in tissues during oxidative stress. As a reactive aldehyde, it forms Michael adducts with nucleophiles, a process that disrupts cellular functioning. Liver, lung and brain are highly sensitive to xenobiotic-induced oxidative stress and readily generate 4-HNE. In the present studies, we compared 4-HNE metabolism in these tissues, a process that protects against tissue injury. 4-HNE was degraded slowly in total homogenates and S9 fractions of mouse liver, lung and brain. In liver, but not lung or brain, NAD(P)+ and NAD(P)H markedly stimulated 4-HNE metabolism. Similar results were observed in rat S9 fractions from these tissues. In liver, lung and brain S9 fractions, 4-HNE formed protein adducts. When NADH was used to stimulate 4-HNE metabolism, the formation of protein adducts was suppressed in liver, but not lung or brain. In both mouse and rat tissues, 4-HNE was also metabolized by glutathione S-transferases. The greatest activity was noted in livers of mice and in lungs of rats; relatively low glutathione S-transferase activity was detected in brain. In mouse hepatocytes, 4-HNE was rapidly taken up and metabolized. Simultaneously, 4-HNE-protein adducts were formed, suggesting that 4-HNE metabolism in intact cells does not prevent protein modifications. These data demonstrate that, in contrast to liver, lung and brain have a limited capacity to metabolize 4-HNE. The persistence of 4-HNE in these tissues may increase the likelihood of tissue injury during oxidative stress.
[Display omitted]
•Lipid peroxidation generates 4-hydroxynonenal, a highly reactive aldehyde.•Rodent liver, but not lung or brain, is efficient in degrading 4-hydroxynonenal.•4-hydroxynonenal persists in tissues with low metabolism, causing tissue damage.</abstract><cop>Amsterdam</cop><pub>Elsevier Inc</pub><pmid>24832492</pmid><doi>10.1016/j.taap.2014.04.026</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 4-Hydroxynonenal 60 APPLIED LIFE SCIENCES ALCOHOL DEHYDROGENASE Aldehydes - antagonists & inhibitors Aldehydes - metabolism ANIMAL TISSUES Animals Antibodies, Blocking - pharmacology Biological and medical sciences Blotting, Western BRAIN Brain - drug effects Brain - enzymology Brain - metabolism Enzyme Inhibitors - pharmacology GLUTATHIONE Glutathione Transferase - antagonists & inhibitors Glutathione Transferase - metabolism Hepatocytes - drug effects Hepatocytes - metabolism HOMOGENATES INJURIES Kinetics Lipid peroxidation LIPIDS LIVER Liver - drug effects Liver - enzymology Liver - metabolism LIVER CELLS Lung - drug effects Lung - enzymology Lung - metabolism LUNGS Male Medical sciences METABOLISM MICE Mice, Inbred C57BL NAD Neurotoxicity OXIDATION Pulmonary toxicity RATS Rats, Long-Evans Reactive oxygen species Species Specificity STRESSES Subcellular Fractions - enzymology Subcellular Fractions - metabolism TOXICITY Toxicology TRANSFERASES |
title | Differential metabolism of 4-hydroxynonenal in liver, lung and brain of mice and rats |
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