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Mountain‐top mining particulate matter exposure increases markers of mitochondrially‐driven apoptosis in rat cardiac tissue
Author(s) -
Nichols Cody Edward,
Baseler Walter A.,
Thapa Dharendra,
LaFata Gabrielle,
Croston Tara L.,
Shepherd Danielle L.,
Lewis Sara E.,
Knuckles Travis L.,
McCawley Michael,
Hendryx Michael,
Nurkiewicz Timothy R.,
Hollander John M.
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1036.15
Subject(s) - apoptosis , downregulation and upregulation , mitochondrial permeability transition pore , chemistry , caspase 3 , particulates , medicine , endocrinology , microbiology and biotechnology , biology , programmed cell death , biochemistry , organic chemistry , gene
Particulate matter (PM) exposure has been associated with adverse health effects in many different regions throughout the US. In the Appalachian region, research has shown that there is a higher incidence of chronic cardiovascular disease in regions with local mountain‐top mining (MTM) operations. The goal of this study was to determine the effect of MTM PM exposure on cellular apoptotic pathways within the heart. Sprague Dawley rats were exposed to MTM PM, collected within one mile of an active MTM site, through intratracheal instillation and heart tissue examined. Bax/Bcl‐2 ratio was significantly increased in exposed rats relative to control (p<0.05) suggesting an increase in cellular apoptosis. Caspase‐3 and ‐9 activities were significantly increased in exposed rats relative to control (p<0.05) with no change in caspase‐8, suggesting an increase in mitochondrially‐driven apoptosis. Putative mitochondrial permeability transition pore constituent, cyclophillin D, was increased in exposed rats compared to control (p<0.05). These results indicate that mitochondrially‐driven apoptosis is upregulated in the heart following MTM PM exposure which may be associated with an increase in a key transition pore constituent. (Support: NIH DP2DK083095, NIH T32HL090610, AHA 10PRE3420006, NIH RO1ES015022, RC1 ES018274 , NIH 5P20RR016477)