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Respiratory effects of hexachlorocyclopentadiene on intact rainbow trout (Salmo gairdneri) and on oxidative phosphorylation of isolated trout heart mitochondria

dc.contributor.authorSinhaseni, Palarpen_US
dc.contributor.authorD'Alecy, Louis G.en_US
dc.contributor.authorHartung, Rolfen_US
dc.contributor.authorShlafer, Marshalen_US
dc.date.accessioned2006-04-07T18:45:54Z
dc.date.available2006-04-07T18:45:54Z
dc.date.issued1983-02en_US
dc.identifier.citationSinhaseni, Palarp, D'Alecy, Louis G., Hartung, Rolf, Shlafer, Marshal (1983/02)."Respiratory effects of hexachlorocyclopentadiene on intact rainbow trout (Salmo gairdneri) and on oxidative phosphorylation of isolated trout heart mitochondria." Toxicology and Applied Pharmacology 67(2): 215-223. <http://hdl.handle.net/2027.42/25308>en_US
dc.identifier.urihttp://www.sciencedirect.com/science/article/B6WXH-4DDPYDV-15/2/35e1062024b292b200465ccbee42fb9cen_US
dc.identifier.urihttps://hdl.handle.net/2027.42/25308
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=6836575&dopt=citationen_US
dc.description.abstractAcclimated normal rainbow trout were exposed to 130 ppb hexachlorocyclopentadiene (HEX) in a flow-through well water circuit which was designed to permit measurements of oxygen consumption by the fish. Compared to preHEX values, HEX increased oxygen consumption rates by 186 +/- 24% (), with maximum oxygen consumption rates being reached in approximately 84 min after HEX exposure. Oxygen consumption subsequently decreased, and all HEX-exposed fish died within 6.5 hr of exposure. Fish exposed to HEX-free vehicle (acetone) showed no changes of oxygen consumption. When added to normal isolated trout heart mitochondria, HEX appeared to uncouple oxidative phosphorylation, with calculated respiratory control ratios being decreased 50% from control values at a HEX concentration of 0.41 [mu]. We postulate that one important mechanism of HEX intoxication in the intact animal may be due to increased oxygen consumption and impaired oxidative ATP synthesis due to the mitochondrial uncoupling action of the toxicant.en_US
dc.format.extent755399 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.language.isoen_US
dc.publisherElsevieren_US
dc.titleRespiratory effects of hexachlorocyclopentadiene on intact rainbow trout (Salmo gairdneri) and on oxidative phosphorylation of isolated trout heart mitochondriaen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelPublic Healthen_US
dc.subject.hlbsecondlevelPharmacy and Pharmacologyen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumInstitute of Environmental and Industrial Health, University of Michigan Medical School, Ann Arbor, Michigan 48109, USAen_US
dc.contributor.affiliationumDepartment of Physiology, University of Michigan Medical School, Ann Arbor, Michigan 48109, USAen_US
dc.contributor.affiliationumInstitute of Environmental and Industrial Health, University of Michigan Medical School, Ann Arbor, Michigan 48109, USAen_US
dc.contributor.affiliationumDepartment of Pharmacology, University of Michigan Medical School, Ann Arbor, Michigan 48109, USAen_US
dc.identifier.pmid6836575en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/25308/1/0000753.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1016/0041-008X(83)90227-2en_US
dc.identifier.sourceToxicology and Applied Pharmacologyen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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