Maternal titanium dioxide nanomaterial inhalation exposure compromises placental hemodynamics
| Autor: | Elizabeth C. Bowdridge, Timothy R. Nurkiewicz, Alaeddin B. Abukabda, Sherri Friend, Thomas P. Batchelor, William T. Goldsmith, Krista L Garner, Carroll R. McBride |
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| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Placenta Metal Nanoparticles Toxicology Article Rats Sprague-Dawley 03 medical and health sciences 0302 clinical medicine Pregnancy Internal medicine medicine.artery Animals Medicine Titanium Pharmacology Inhalation exposure Inhalation Exposure Fetus Lung Inhalation business.industry technology industry and agriculture Hemodynamics Umbilical artery Angiotensin II 030104 developmental biology medicine.anatomical_structure Endocrinology Maternal Exposure 030220 oncology & carcinogenesis Vascular resistance Female business |
| Zdroj: | Toxicology and Applied Pharmacology. 367:51-61 |
| ISSN: | 0041-008X |
| Popis: | The fetal consequences of gestational engineered nanomaterial (ENM) exposure are unclear. The placenta is a barrier protecting the fetus and allowing transfer of substances from the maternal circulation. The purpose of this study was to determine the effects of maternal pulmonary titanium dioxide nanoparticle (nano-TiO(2)) exposure on the placenta and umbilical vascular reactivity. We hypothesized that pulmonary nano-TiO(2) inhalation exposure increases placental vascular resistance and impairs umbilical vascular responsiveness. Pregnant Sprague-Dawley rats were exposed via whole-body inhalation to nano-TiO(2) with an aerodynamic diameter of 188 ± 0.36 nm. On gestational day (GD) 11, rats began inhalation exposures (6h/exposure). Daily lung deposition was 87.5 ± 2.7 μg. Animals were exposed for 6 days for a cumulative lung burden of 525 ± 16 μg. On GD 20, placentas, umbilical artery and vein were isolated, cannulated, and treated with acetylcholine (ACh), angiotensin II (ANGII), S-nitroso-N-acetyl-DL-penicillamine (SNAP), or calcium-free superfusate (Ca(2+)-free). Mean outflow pressure was measured in placental units. ACh increased outflow pressure to 53 ± 5 mm Hg in sham-controls but only to 35 ± 4 mm Hg in exposed subjects. ANGII decreased outflow pressure in placentas from exposed animals (17 ± 7 mm Hg) compared to sham-controls (31 ± 6 mm Hg). Ca(2+)-free superfusate yielded maximal outflow pressures in sham-control (63 ± 5 mm Hg) and exposed (30 ± 10 mm Hg) rats. Umbilical artery endothelium-dependent dilation was decreased in nano-TiO(2) exposed fetuses (30 ± 9%) compared to sham-controls (58 ± 6%), but ANGII sensitivity was increased (−79 ± 20% vs −36 ± 10%). These results indicate that maternal gestational pulmonary nano-TiO(2) exposure increases placental vascular resistance and impairs umbilical vascular reactivity. |
| Databáze: | OpenAIRE |
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