Premium
Acute Inhalation Exposure of Nano‐Titanium Dioxide induces Cardiac and Mitochondrial Dysfunction in Mice
Author(s) -
Nichols Cody,
Shepherd Danielle,
Croston Tara,
Thapa Dharendra,
Lewis Sara,
Jagannathan Rajaganapathi,
Yi Jinhai,
Nurkiewicz Timothy,
Hollander John
Publication year - 2013
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.27.1_supplement.890.9
Subject(s) - inhalation , mitochondrion , cardiac function curve , inhalation exposure , diastole , cardiac dysfunction , chemistry , diastolic function , medicine , cardiology , andrology , toxicology , physiology , biology , anesthesia , heart failure , biochemistry , blood pressure
While nanotechnology offers innovation in products from cosmetics to drug delivery, exposure to engineered nanomaterial (ENM) is increasing. Unfortunately, health impacts of ENM are not fully realized. Titanium Dioxide (nanoTiO2) is one of the most widely produced ENM due to its variety of uses. The goal of this study was to determine the effects of nanoTiO2 inhalation exposure on cardiac and mitochondrial function. Male FVB mice were exposed to nanoTiO2 at an estimated total lung deposition of 11 μg. Twenty‐four hours after exposure cardiac function was assessed using a Vevo 2100 echocardiography system. Diastolic dysfunction was observed, supported by increased diastolic radial strain, increased E/A ratios (>;2.0), and increased early mitral flow deceleration time (p<0.05, for all three). Inductively coupled plasma atomic emission spectroscopy detected an 80% increase in Ti content in cardiac tissue following exposure suggesting particle translocation as a potential source of cellular stress. To identify subcellular mechanisms mitochondria were isolated and respiration rates assessed. A decrease in active (State 3) respiration rate following exposure was observed (p<0.05). In summary, nanoTiO2 inhalation exposure is associated with cardiac diastolic dysfunction and mitochondrial functional alterations. (Supported by NIH DP2DK08309, NIH R01ES015022, RC1 ES018274, DGE‐1144676, NIH T32HL090610)