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Spatially-distinct cardiac mitochondrial dysfunction following pulmonary exposure to various carbon-based nanomaterials.

Authors
Nichols-CE; Erdely-A; Shepherd-DL; Thapa-D; Salmen-R; McLoughlin-CE; Sager-TM; Roberts-JR; Hollander-JM
Source
Toxicologist 2014 Mar; 138(1):127
NIOSHTIC No.
20043886
Abstract
While carbon-based nanomaterial use continues to grow, the health effects are not fully realized. Nanomaterial inhalation affects lung mitochondria, but cardiac mitochondrial effects are not well defined. Within the heart, analyses are complicated by the presence of two mitochondrial subpopulations: the subsarcolemmal (SSM), beneath the sarcolemma, and interfibrillar (IFM), between the myofibrils. The current study investigated the impact of pulmonary exposure to various carbon-based nanomaterials on the function of cardiac mitochondrial subpopulations. Male C57BL/6 mice were exposed using pharyngeal aspiration to either 40 mg of <2 mm x <2 mm x 1-2 nm graphene (GP-1), 5 mm x 5 mm x 7 nm (GP-5), multi-walled carbon nanotubes (MWCNT), or carbon black; 10 mg of MWCNT; or sham, dispersion media. Four or 24 h after exposure, cardiac mitochondrial subpopulations were isolated and run through polarographic assessments for mitochondrial oxygen consumption. Mitochondrial hydrogen peroxide (H2O2) production was measured using the fluorescent dye Amplex red. The IFM of mice exposed to GP-1 had decreased active respiration 24 h after exposure compared to shams (P<0.05). Exposure to GP-1, GP-5, and carbon black increased IFM H2O2 production compared to shams 4 h post-exposure (P<0.05). Both doses of MWCNT decreased active respiration rates in the IFM at 4 h compared to controls (P<0.05), but no difference at 24 h. Increased production of IFM H2O2 were seen 24 h after exposure to 40 mg MWCNT as compared to shams (P<0.05). No effects were observed in any SSM population. In conclusion, cardiac mitochondrial dysfunction was observed solely in the IFM following pulmonary exposure to carbon-based nanomaterials. Decreased function and increased H2O2 production in the mitochondria between the myofibrils can promote cardiovascular dysfunction.
Keywords
Toxicology; Cell-function; Cellular-function; Toxic-effects; Laboratory-animals; Animals; Cell-damage; Nanotechnology; Lung; Cardiac-function; Exposure-levels; Pulmonary-disorders; Pulmonary-function; Pulmonary-system; Pulmonary-system-disorders
CAS No.
7440-44-0
Publication Date
20140301
Document Type
Abstract
Fiscal Year
2014
NTIS Accession No.
NTIS Price
Identifying No.
M032014
Issue of Publication
1
ISSN
1096-6080
NIOSH Division
HELD
Priority Area
Manufacturing
Source Name
The Toxicologist. Society of Toxicology 53rd Annual Meeting and ToxExpo, March 23-27, 2014, Phonex, Arizona
State
WV
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