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dc.contributor.author배옥남-
dc.date.accessioned2019-06-03T07:45:06Z-
dc.date.available2019-06-03T07:45:06Z-
dc.date.issued2007-01-
dc.identifier.citationCHEMICAL RESEARCH IN TOXICOLOGY, v. 20, No. 1, Page. 38-43en_US
dc.identifier.issn0893-228X-
dc.identifier.issn1520-5010-
dc.identifier.urihttps://pubs.acs.org/doi/full/10.1021/tx060114+-
dc.identifier.urihttps://repository.hanyang.ac.kr/handle/20.500.11754/106230-
dc.description.abstractLead (Pb) is a ubiquitous heavy metal pollutant in various environmental media, especially in food and drinking water. In human blood, about 95% of lead is associated with erythrocytes, suggesting that erythrocytes could be an important target of lead toxicity in the cardiovascular system. Recent studies suggested that erythrocytes could contribute to blood coagulation via phosphatidylserine (PS) exposure and resultant procoagulant activation. We investigated the effects of lead on the procoagulant activity of erythrocytes using in vitro human erythrocyte and in vivo rat models. In a flow cytometric analysis, lead (Pb2+) enhanced PS exposure on human erythrocytes in a concentration- and time-dependent manner. The concentration of lead (1-5 mu M) used in the current investigation is well within the ranges observed in blood from lead-exposed populations. PS exposure by lead appeared to be mediated by increased intracellular calcium levels as shown by F-19-NMR and intracellular ATP depletion. Consistent with these findings, the activity of scramblase, which is important in the induction of PS exposure, was enhanced, whereas the activity of flippase, which translocates exposed PS to inner membrane, was inhibited by lead treatment. Furthermore, lead-exposed erythrocytes increased thrombin generation as determined by a prothrombinase assay and accelerated the coagulation process initiated by tissue factor in plasma. These procoagulant activations by lead were also confirmed in vivo. Administration of lead significantly enhanced PS exposure on erythrocytes and, more importantly, elevated thrombus formation in a rat venous thrombosis model. These results suggest that lead exposure can provoke procoagulant activity in erythrocytes by PS exposure, contributing to enhanced clot formation. These data will provide new insights into the mechanism of lead-induced cardiovascular diseases.en_US
dc.description.sponsorshipThis work was supported by Korea Research Foundation Grant funded by the Korean Government (MOEHRD) (KRF-2006-E00162).en_US
dc.language.isoen_USen_US
dc.publisherAMER CHEMICAL SOCen_US
dc.subjectOSTEOBLASTIC BONE-CELLSen_US
dc.subjectF-19 NMRen_US
dc.subjectSUPEROXIDE-DISMUTASEen_US
dc.subjectLIPID-PEROXIDATIONen_US
dc.subjectBLOOD-PRESSUREen_US
dc.subjectWORKERSen_US
dc.subjectHYPERTENSIONen_US
dc.subjectGENERATIONen_US
dc.subjectMEMBRANESen_US
dc.subjectANAEMIAen_US
dc.titleLead-induced procoagulant activation of erythrocytes through phosphatidylserine exposure may lead to thrombotic diseasesen_US
dc.typeArticleen_US
dc.relation.volume20-
dc.identifier.doi10.1021/tx060114+-
dc.relation.page38-43-
dc.relation.journalCHEMICAL RESEARCH IN TOXICOLOGY-
dc.contributor.googleauthorShin, Jung-Hun-
dc.contributor.googleauthorLim, Kyung-Min-
dc.contributor.googleauthorNoh, Ji-Yoon-
dc.contributor.googleauthorBae, Ok-Nam-
dc.contributor.googleauthorChung, Seung-Min-
dc.contributor.googleauthorLee, Moo-Yeol-
dc.contributor.googleauthorChung, Jin-Ho-
dc.relation.code2007201814-
dc.sector.campusE-
dc.sector.daehakCOLLEGE OF PHARMACY[E]-
dc.sector.departmentDEPARTMENT OF PHARMACY-
dc.identifier.pidonbae-
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COLLEGE OF PHARMACY[E](약학대학) > PHARMACY(약학과) > Articles
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