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Maternal-engineered nanomaterial exposure disrupts progeny cardiac function and bioenergetics

Quincy A. Hathaway, C.E. Nichols, Danielle L. Shepherd, Phoebe A. Stapleton, Sarah L. McLaughlin, Janelle Stricker, Stephanie L. Rellick, Mark V. Pinti, Alaeddin B. Abukabda, Carroll McBride, Jinghai Yi, Seth M. Stine, Timothy R. Nurkiewicz, John M. Hollander

American Journal of Physiology-Heart and Circulatory Physiology · 2016 · ▲ 80 citations

Abstract

Nanomaterial production is expanding as new industrial and consumer applications are introduced. Nevertheless, the impacts of exposure to these compounds are not fully realized. The present study was designed to determine whether gestational nano-sized titanium dioxide exposure impacts cardiac and metabolic function of developing progeny. Pregnant Sprague-Dawley rats were exposed to nano-aerosols (~10 mg/m 3 , 130- to 150-nm count median aerodynamic diameter) for 7–8 nonconsecutive days, beginning at gestational day 5–6. Physiological and bioenergetic effects on heart function and cardiomyocytes across three time points, fetal (gestational day 20), neonatal (4–10 days), and young adult (6–12 wk), were evaluated. Functional analysis utilizing echocardiography, speckle-tracking based strain, and cardiomyocyte contractility, coupled with mitochondrial energetics, revealed effects of nano-exposure. Maternal exposed progeny demonstrated a decrease in E- and A-wave velocities, with a 15% higher E-to-A ratio than controls. Myocytes isolated from exposed animals exhibited ~30% decrease in total contractility, departure velocity, and area of contraction. Bioenergetic analysis revealed a significant increase in proton leak across all ages, accompanied by decreases in metabolic function, including basal respiration, maximal respiration, and spare capacity. Finally, electron transport chain complex I and IV activities were negatively impacted in the exposed group, which may be linked to a metabolic shift. Molecular data suggest that an increase in fatty acid metabolism, uncoupling, and cellular stress proteins may be associated with functional deficits of the heart. In conclusion, gestational nano-exposure significantly impairs the functional capabilities of the heart through cardiomyocyte impairment, which is associated with mitochondrial dysfunction(definition). NEW & NOTEWORTHY Cardiac function is evaluated, for the first time, in progeny following maternal nanomaterial inhalation. The findings indicate that exposure to nano-sized titanium dioxide (nano-TiO 2 ) during gestation negatively impacts cardiac function and mitochondrial respiration and bioenergetics. We conclude that maternal nano-TiO 2 inhalation contributes to adverse cardiovascular health effects, lasting into adulthood. Listen to this article's corresponding podcast at https://ajpheart.podbean.com/e/gestational-nanomaterial-exposure-and-cardiac-dysfunction/ .

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Provenance

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OpenAlex
DOI
10.1152/ajpheart.00634.2016
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2026-06-01 MST

Cite this

APA
Hathaway, Q.A., Nichols, C., Shepherd, D.L., Stapleton, P.A., McLaughlin, S.L., Stricker, J., Rellick, S.L., Pinti, M.V., Abukabda, A.B., McBride, C., Yi, J., Stine, S.M., Nurkiewicz, T.R., &amp; Hollander, J.M. (2016). Maternal-engineered nanomaterial exposure disrupts progeny cardiac function and bioenergetics. <em>American Journal of Physiology-Heart and Circulatory Physiology</em>. https://doi.org/10.1152/ajpheart.00634.2016
Vancouver
Hathaway QA, Nichols C, Shepherd DL, Stapleton PA, McLaughlin SL, Stricker J, et al. Maternal-engineered nanomaterial exposure disrupts progeny cardiac function and bioenergetics. American Journal of Physiology-Heart and Circulatory Physiology. 2016. doi:10.1152/ajpheart.00634.2016.
BibTeX
@article{quincy2016Matern, title = {Maternal-engineered nanomaterial exposure disrupts progeny cardiac function and bioenergetics}, author = {Quincy A. Hathaway and C.E. Nichols and Danielle L. Shepherd and Phoebe A. Stapleton and Sarah L. McLaughlin and Janelle Stricker and Stephanie L. Rellick and Mark V. Pinti and Alaeddin B. Abukabda and Carroll McBride and Jinghai Yi and Seth M. Stine and Timothy R. Nurkiewicz and John M. Hollander}, journal = {American Journal of Physiology-Heart and Circulatory Physiology}, year = {2016}, doi = {10.1152/ajpheart.00634.2016}, }

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