Oxidative stress, endothelial dysfunction and inflammatory response in rat heart to NO₂ inhalation exposure.

Abstract

Epidemiological studies suggest that NO₂ inhalation is associated with adverse effects on heart-related health, however, existing experimental data lack relevant evidences. In this study, a role for oxidative stress, endothelial dysfunction and inflammatory responses in the heart of rats treated with different concentrations of NO₂ (0, 5, 10 and 20 mg m⁻³) was investigated. Mild heart pathology occurred after 7-d exposure (6 h d⁻¹). Marked oxidative stress were induced as evaluated by reduction/induction of antioxidants (Cu/Zn-SOD, Mn-SOD and GPx) activity and increasing formation of MDA and PCO. Also, mRNA and protein biomarkers of vasoconstriction (ET-1, eNOS) and inflammation (TNF-α, IL-1β and ICAM-1) were up-regulated, and p53 mRNA expression, bax/bcl-2 ratio and the mean number of TUNEL-positive myocytes were increased as well. All the results implicate that NO₂ exerted injuries to mammals' heart, and the damage mechanisms were possibly associated with oxidative stress, endothelial dysfunction and inflammation.

DOI: 10.1016/j.chemosphere.2010.11.055
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@article{Li2011OxidativeSE, title={Oxidative stress, endothelial dysfunction and inflammatory response in rat heart to NO₂ inhalation exposure.}, author={Hongyan Li and Ming Han and Lin Guo and Guangke Li and Nan Sang}, journal={Chemosphere}, year={2011}, volume={82 11}, pages={1589-96} }