Abstract：
:Epidemiological studies have associated air pollution particulate matter (PM) exposure with adverse cardiovascular effects. Identification of causal PM sources is critically needed to support regulatory decisions to protect public health. This research examines the in vitro cardiotoxicity of bioavailable constituents of residual oil fly ash (ROFA) employing in vivo, biokinetically-based, concentrations determined from their pulmonary deposition. Pulmonary deposition of ROFA led to a rapid increase in plasma vanadium (V) levels that were prolonged in hypertensive animals without systemic inflammation. ROFA cardiotoxicity was evaluated using neonatal rat cardiomyocyte (RCM) cultures exposed to particle-free leachates of ROFA (ROFA-L) at levels present in exposed rat plasma. Cardiotoxicity was observed at low levels (3.13 μg/mL) of ROFA-L 24 h post-exposure. Dimethylthiourea (28 mM) inhibited ROFA-L-induced cytotoxicity at high (25-12.5 μg/mL) doses, suggesting that oxidative stress is responsible at high ROFA-L doses. Cardiotoxicity could not be reproduced using a V + Ni + Fe mixture or a ROFA-L depleted of these metals, suggesting that ROFA-L cardiotoxicity requires the full complement of bioavailable constituents. Susceptibility of RCMs to ROFA-L-induced cytotoxicity was increased following tyrosine phosphorylation inhibition, suggesting that phosphotyrosine signaling pathways play a critical role in regulating ROFA-L-induced cardiotoxicity. These data demonstrate that bioavailable constituents of ROFA are capable of direct adverse cardiac effects.
journal_name
Cardiovasc Toxicoljournal_title
Cardiovascular toxicologyauthors
Knuckles TL,Jaskot R,Richards JH,Miller CA,Ledbetter A,McGee J,Linak WP,Dreher KLdoi
10.1007/s12012-013-9225-zsubject
Has Abstractpub_date
2013-12-01 00:00:00pages
426-37issue
4eissn
1530-7905issn
1559-0259journal_volume
13pub_type
杂志文章abstract：:The use of anthracycline anticancer drugs is limited by a cumulative, dose-dependent cardiac toxicity. Iron chelation has long been considered as a promising strategy to limit this unfavorable side effect, either by restoring the disturbed cellular iron homeostasis or by removing redox-active iron, which may promote a...
journal_title：Cardiovascular toxicology
pub_type： 杂志文章,评审
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journal_title：Cardiovascular toxicology
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journal_title：Cardiovascular toxicology
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journal_title：Cardiovascular toxicology
pub_type： 杂志文章
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journal_title：Cardiovascular toxicology
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journal_title：Cardiovascular toxicology
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journal_title：Cardiovascular toxicology
pub_type： 杂志文章
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更新日期：2011-06-01 00:00:00
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journal_title：Cardiovascular toxicology
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journal_title：Cardiovascular toxicology
pub_type： 杂志文章
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更新日期：2016-04-01 00:00:00
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journal_title：Cardiovascular toxicology
pub_type： 杂志文章
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更新日期：2011-03-01 00:00:00
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journal_title：Cardiovascular toxicology
pub_type： 杂志文章,评审
doi：10.1007/s12012-007-0004-6
更新日期：2007-01-01 00:00:00
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journal_title：Cardiovascular toxicology
pub_type： 杂志文章
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journal_title：Cardiovascular toxicology
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journal_title：Cardiovascular toxicology
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journal_title：Cardiovascular toxicology
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journal_title：Cardiovascular toxicology
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journal_title：Cardiovascular toxicology
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journal_title：Cardiovascular toxicology
pub_type： 杂志文章
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更新日期：2002-01-01 00:00:00
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journal_title：Cardiovascular toxicology
pub_type： 杂志文章
doi：10.1385/ct:3:4:331
更新日期：2003-01-01 00:00:00
abstract：:It has been suggested that prenatal exposure to cadmium may alter the cardiovascular function during adulthood. Using the left coronary artery ligation model of acute myocardial infarction, we studied the cardiac function of female adult offspring rats exposed to cadmium (30 ppm) during gestation. The cardiac ischemic...
journal_title：Cardiovascular toxicology
pub_type： 杂志文章
doi：10.1007/s12012-011-9139-6
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